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  Subjects -> BIOLOGY (Total: 3003 journals)
    - BIOCHEMISTRY (237 journals)
    - BIOENGINEERING (108 journals)
    - BIOLOGY (1427 journals)
    - BIOPHYSICS (46 journals)
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    - ORNITHOLOGY (25 journals)
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    - ZOOLOGY (133 journals)

BIOCHEMISTRY (237 journals)                  1 2 | Last

Showing 1 - 200 of 237 Journals sorted alphabetically
AAPS PharmSciTech     Hybrid Journal   (Followers: 6)
Acetic Acid Bacteria     Open Access   (Followers: 2)
ACS Central Science     Open Access   (Followers: 7)
ACS Chemical Biology     Full-text available via subscription   (Followers: 254)
ACS Chemical Neuroscience     Full-text available via subscription   (Followers: 18)
Acta Biochimica Polonica     Open Access  
Acta Crystallographica Section D : Biological Crystallography     Hybrid Journal   (Followers: 9)
Acta Crystallographica Section F: Structural Biology Communications     Hybrid Journal   (Followers: 8)
Advances and Applications in Bioinformatics and Chemistry     Open Access   (Followers: 10)
Advances in Biological Chemistry     Open Access   (Followers: 7)
Advances in Carbohydrate Chemistry and Biochemistry     Full-text available via subscription   (Followers: 9)
Advances in Plant Biochemistry and Molecular Biology     Full-text available via subscription   (Followers: 8)
Advances in Protein Chemistry and Structural Biology     Full-text available via subscription   (Followers: 20)
African Journal of Biochemistry Research     Open Access   (Followers: 1)
African Journal of Chemical Education     Open Access   (Followers: 2)
Alkaloids: Chemical and Biological Perspectives     Full-text available via subscription   (Followers: 3)
American Journal of Biochemistry     Open Access   (Followers: 8)
American Journal of Biochemistry and Biotechnology     Open Access   (Followers: 67)
American Journal of Biochemistry and Molecular Biology     Open Access   (Followers: 14)
American Journal of Polymer Science     Open Access   (Followers: 25)
Amino Acids     Hybrid Journal   (Followers: 8)
Analytical and Bioanalytical Chemistry Research     Open Access  
Analytical Biochemistry     Hybrid Journal   (Followers: 166)
Angiogenesis     Hybrid Journal   (Followers: 3)
Annals of Clinical Biochemistry     Hybrid Journal   (Followers: 8)
Annual Review of Biochemistry     Full-text available via subscription   (Followers: 55)
Annual Review of Chemical and Biomolecular Engineering     Full-text available via subscription   (Followers: 12)
Applied Biochemistry and Biotechnology     Hybrid Journal   (Followers: 44)
Applied Biochemistry and Microbiology     Hybrid Journal   (Followers: 17)
Applied Organometallic Chemistry     Hybrid Journal   (Followers: 7)
Archives of Biochemistry and Biophysics     Hybrid Journal   (Followers: 20)
Archives of Insect Biochemistry and Physiology     Hybrid Journal  
Archives Of Physiology And Biochemistry     Hybrid Journal   (Followers: 1)
Asian Journal of Biochemistry     Open Access   (Followers: 1)
Bangladesh Journal of Medical Biochemistry     Open Access   (Followers: 3)
BBA Clinical     Open Access  
BBR : Biochemistry and Biotechnology Reports     Open Access   (Followers: 4)
Biocatalysis     Open Access  
Biochemical and Biophysical Research Communications     Hybrid Journal   (Followers: 21)
Biochemical and Molecular Medicine     Full-text available via subscription   (Followers: 4)
Biochemical Compounds     Open Access  
Biochemical Engineering Journal     Hybrid Journal   (Followers: 14)
Biochemical Genetics     Hybrid Journal   (Followers: 3)
Biochemical Journal     Full-text available via subscription   (Followers: 25)
Biochemical Pharmacology     Hybrid Journal   (Followers: 10)
Biochemical Society Transactions     Full-text available via subscription   (Followers: 4)
Biochemical Systematics and Ecology     Hybrid Journal   (Followers: 3)
Biochemistry     Full-text available via subscription   (Followers: 304)
Biochemistry & Pharmacology : Open Access     Open Access   (Followers: 3)
Biochemistry & Physiology : Open Access     Open Access  
Biochemistry (Moscow)     Hybrid Journal   (Followers: 4)
Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology     Hybrid Journal   (Followers: 3)
Biochemistry (Moscow) Supplemental Series B: Biomedical Chemistry     Hybrid Journal   (Followers: 3)
Biochemistry and Biophysics Reports     Open Access  
Biochemistry and Cell Biology     Hybrid Journal   (Followers: 14)
Biochemistry and Molecular Biology Education     Hybrid Journal   (Followers: 6)
Biochemistry and Molecular Biology of Fishes     Full-text available via subscription   (Followers: 1)
Biochemistry Research International     Open Access   (Followers: 6)
Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids     Hybrid Journal   (Followers: 7)
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease     Hybrid Journal   (Followers: 14)
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research     Hybrid Journal   (Followers: 9)
Biochimie     Hybrid Journal   (Followers: 7)
Biochimie Open     Open Access  
Bioconjugate Chemistry     Full-text available via subscription   (Followers: 30)
BioDrugs     Full-text available via subscription   (Followers: 7)
Bioelectrochemistry     Hybrid Journal   (Followers: 2)
Biofuels     Hybrid Journal   (Followers: 11)
Biogeochemistry     Hybrid Journal   (Followers: 14)
BioInorganic Reaction Mechanisms     Hybrid Journal   (Followers: 1)
Biokemistri     Open Access  
Biological Chemistry     Partially Free   (Followers: 22)
Biomaterials Research     Open Access   (Followers: 4)
Biomedicines     Open Access   (Followers: 1)
BioMolecular Concepts     Hybrid Journal   (Followers: 2)
Bioscience, Biotechnology, and Biochemistry     Hybrid Journal   (Followers: 24)
Biosimilars     Open Access   (Followers: 1)
Biotechnology and Applied Biochemistry     Hybrid Journal   (Followers: 45)
Bitácora Digital     Open Access  
BMC Biochemistry     Open Access   (Followers: 14)
Bulletin of University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca : Food Science and Technology     Open Access   (Followers: 1)
Carbohydrate Polymers     Hybrid Journal   (Followers: 8)
Cell Biochemistry and Biophysics     Hybrid Journal   (Followers: 6)
Cell Biochemistry and Function     Hybrid Journal   (Followers: 6)
Cellular Physiology and Biochemistry     Open Access   (Followers: 3)
ChemBioChem     Hybrid Journal   (Followers: 7)
Chemical and Biological Technologies for Agriculture     Open Access  
Chemical Biology & Drug Design     Hybrid Journal   (Followers: 20)
Chemical Engineering Journal     Hybrid Journal   (Followers: 45)
Chemical Senses     Hybrid Journal   (Followers: 1)
Chemical Speciation and Bioavailability     Open Access   (Followers: 1)
Chemico-Biological Interactions     Hybrid Journal   (Followers: 3)
Chemistry & Biodiversity     Hybrid Journal   (Followers: 6)
Chemistry & Biology     Full-text available via subscription   (Followers: 30)
Chemistry and Ecology     Hybrid Journal  
ChemTexts     Hybrid Journal  
Clinica Chimica Acta     Hybrid Journal   (Followers: 33)
Clinical Biochemist Reviews     Full-text available via subscription   (Followers: 1)
Clinical Biochemistry     Hybrid Journal   (Followers: 18)
Clinical Chemistry     Full-text available via subscription   (Followers: 68)
Clinical Chemistry and Laboratory Medicine     Hybrid Journal   (Followers: 61)
Clinical Lipidology     Full-text available via subscription   (Followers: 1)
Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology     Hybrid Journal   (Followers: 4)
Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology     Hybrid Journal   (Followers: 1)
Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology     Hybrid Journal   (Followers: 7)
Comparative Biochemistry and Physiology Part D: Genomics and Proteomics     Hybrid Journal   (Followers: 2)
Comprehensive Biochemistry     Full-text available via subscription   (Followers: 1)
Computational Biology and Chemistry     Hybrid Journal   (Followers: 12)
Critical Reviews in Biochemistry and Molecular Biology     Hybrid Journal   (Followers: 5)
Current Chemical Biology     Hybrid Journal   (Followers: 2)
Current Medicinal Chemistry     Hybrid Journal   (Followers: 16)
Current Opinion in Chemical Biology     Hybrid Journal   (Followers: 28)
Current Opinion in Lipidology     Hybrid Journal   (Followers: 6)
DNA Barcodes     Open Access  
Doklady Biochemistry and Biophysics     Hybrid Journal   (Followers: 1)
Doklady Chemistry     Hybrid Journal  
Egyptian Journal of Biochemistry and Molecular Biology     Full-text available via subscription  
FABICIB     Open Access  
FEBS Letters     Hybrid Journal   (Followers: 56)
FEBS Open Bio     Open Access   (Followers: 3)
Fish Physiology and Biochemistry     Hybrid Journal   (Followers: 4)
Food & Function     Full-text available via subscription   (Followers: 5)
Foundations of Modern Biochemistry     Full-text available via subscription  
Free Radicals and Antioxidants     Full-text available via subscription   (Followers: 4)
Frontiers in Molecular Biosciences     Open Access   (Followers: 2)
Frontiers in Natural Product Chemistry     Hybrid Journal  
Global Biogeochemical Cycles     Full-text available via subscription   (Followers: 15)
Green Chemistry     Full-text available via subscription   (Followers: 10)
Histochemistry and Cell Biology     Hybrid Journal   (Followers: 5)
Indian Journal of Biochemistry and Biophysics (IJBB)     Open Access   (Followers: 3)
Indian Journal of Clinical Biochemistry     Hybrid Journal   (Followers: 1)
Indonesian Biomedical Journal     Open Access  
Insect Biochemistry and Molecular Biology     Hybrid Journal   (Followers: 3)
International Journal of Biochemistry & Cell Biology     Hybrid Journal   (Followers: 8)
International Journal of Biochemistry and Biophysics     Open Access   (Followers: 1)
International Journal of Biological Chemistry     Open Access   (Followers: 4)
International Journal of Biomedical Nanoscience and Nanotechnology     Hybrid Journal   (Followers: 6)
International Journal of Food Contamination     Open Access  
International Journal of Plant Physiology and Biochemistry     Open Access   (Followers: 1)
International Journal of Plant Research     Open Access   (Followers: 3)
International Journal of Secondary Metabolite     Open Access   (Followers: 1)
Invertebrate Immunity     Open Access   (Followers: 1)
JBIC Journal of Biological Inorganic Chemistry     Hybrid Journal   (Followers: 4)
Journal of Microbial & Biochemical Technology     Open Access   (Followers: 2)
Journal of Applied Biology & Biotechnology     Open Access   (Followers: 2)
Journal of Bioactive and Compatible Polymers     Hybrid Journal   (Followers: 3)
Journal of Biochemistry     Hybrid Journal   (Followers: 43)
Journal of Biochemistry and Molecular Biology Research     Open Access  
Journal of Biological Chemistry     Full-text available via subscription   (Followers: 197)
Journal of Biomaterials Science, Polymer Edition     Hybrid Journal   (Followers: 9)
Journal of Carbohydrate Chemistry     Hybrid Journal   (Followers: 7)
Journal of Cellular Biochemistry     Hybrid Journal   (Followers: 5)
Journal of Chemical Biology     Hybrid Journal   (Followers: 3)
Journal of Chemical Neuroanatomy     Hybrid Journal  
Journal of Clinical Lipidology     Hybrid Journal   (Followers: 1)
Journal of Comparative Physiology B : Biochemical, Systemic, and Environmental Physiology     Hybrid Journal   (Followers: 4)
Journal of Drug Discovery and Therapeutics     Open Access  
Journal of Enzyme Inhibition and Medicinal Chemistry     Open Access   (Followers: 3)
Journal of Evolutionary Biochemistry and Physiology     Hybrid Journal  
Journal of Food and Drug Analysis     Open Access  
Journal of Forensic Toxicology and Pharmacology     Hybrid Journal   (Followers: 4)
Journal of Inborn Errors of Metabolism and Screening     Open Access  
Journal of Inorganic Biochemistry     Hybrid Journal   (Followers: 6)
Journal of Medical and Biomedical Sciences     Open Access  
Journal of Medical Biochemistry     Open Access   (Followers: 4)
Journal of Medicine and Biomedical Research     Open Access   (Followers: 1)
Journal of Molecular Biochemistry     Open Access   (Followers: 3)
Journal of Molecular Diagnostics     Hybrid Journal   (Followers: 6)
Journal of Neurochemistry     Hybrid Journal   (Followers: 4)
Journal of Nutritional Biochemistry     Hybrid Journal   (Followers: 7)
Journal of Pediatric Biochemistry     Hybrid Journal   (Followers: 1)
Journal of Peptide Science     Hybrid Journal   (Followers: 22)
Journal of Photochemistry and Photobiology B: Biology     Hybrid Journal   (Followers: 3)
Journal of Physiobiochemical Metabolism     Hybrid Journal   (Followers: 1)
Journal of Physiology and Biochemistry     Hybrid Journal   (Followers: 3)
Journal of Plant Biochemistry and Biotechnology     Hybrid Journal   (Followers: 6)
Journal of Steroid Biochemistry and Molecular Biology     Hybrid Journal   (Followers: 2)
Journal of Virology & Antiviral Research     Hybrid Journal   (Followers: 5)
Journal of Wood Chemistry and Technology     Hybrid Journal   (Followers: 9)
La Rivista Italiana della Medicina di Laboratorio - Italian Journal of Laboratory Medicine     Hybrid Journal  
Lab on a Chip     Full-text available via subscription   (Followers: 36)
Marine Chemistry     Hybrid Journal   (Followers: 6)
Methods in Enzymology     Full-text available via subscription   (Followers: 11)
Molecular and Biochemical Parasitology     Hybrid Journal   (Followers: 2)
Molecular and Cellular Biochemistry     Hybrid Journal   (Followers: 6)
Molecular Aspects of Medicine     Hybrid Journal   (Followers: 3)
Molecular Informatics     Hybrid Journal   (Followers: 6)
Molecular inhibitors in targeted therapy     Open Access  
Moscow University Chemistry Bulletin     Hybrid Journal   (Followers: 1)
Mycologia     Hybrid Journal  
Mycology : An International Journal on Fungal Biology     Hybrid Journal   (Followers: 5)
Natural Products and Bioprospecting     Open Access   (Followers: 2)
Nature Chemical Biology     Full-text available via subscription   (Followers: 72)
Nature Communications     Open Access   (Followers: 192)
Neurosignals     Open Access  
NOVA     Open Access  
Novelty in Biomedicine     Open Access  
OA Biochemistry     Open Access   (Followers: 1)
OA Inflammation     Open Access  
Ocean Acidification     Open Access   (Followers: 4)
Organic & Biomolecular Chemistry     Full-text available via subscription   (Followers: 88)

        1 2 | Last

Journal Cover Archives of Biochemistry and Biophysics
  [SJR: 1.478]   [H-I: 138]   [20 followers]  Follow
    
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 0003-9861 - ISSN (Online) 1096-0384
   Published by Elsevier Homepage  [3043 journals]
  • Mechanistic insights into EgGST1, a Mu class glutathione S-transferase
           from the cestode parasite Echinococcus granulosus
    • Authors: Paula Arbildi; Lucía Turell; Verónica López; Beatriz Alvarez; Verónica Fernández
      Pages: 15 - 22
      Abstract: Publication date: 1 November 2017
      Source:Archives of Biochemistry and Biophysics, Volume 633
      Author(s): Paula Arbildi, Lucía Turell, Verónica López, Beatriz Alvarez, Verónica Fernández
      Glutathione transferases (GSTs) comprise a major detoxification system in helminth parasites, displaying both catalytic and non-catalytic activities. The kinetic mechanism of these enzymes is complex and depends on the isoenzyme which is being analyzed. Here, we characterized the kinetic mechanism of rEgGST1, a recombinant form of a cytosolic GST from Echinococcus granulosus (EgGST1), which is related to the Mu-class of mammalian enzymes, using the canonical substrates glutathione (GSH) and 1-chloro-2,4-dinitrobenzene (CDNB). Initial rate and product inhibition studies were consistent with a steady-state random sequential mechanism, where both substrates are bound to the enzyme before the products are released. Kinetic constants were also determined (pH 6.5 and 30 °C). Moreover, rEgGST1 lowered the pK a of GSH from 8.71 ± 0.07 to 6.77 ± 0.08, and enzyme-bound GSH reacted with CDNB 1 × 105 times faster than free GSH at pH 7.4. Finally, the dissociation of the enzyme-GSH complex was studied by means of intrinsic fluorescence, as well as that of the complex with the anthelminth drug mebendazole. This is the first report on mechanistic issues related to a helminth parasitic GST.
      Graphical abstract image

      PubDate: 2017-09-04T04:00:59Z
      DOI: 10.1016/j.abb.2017.08.014
      Issue No: Vol. 633 (2017)
       
  • Disulfiram is a slow-binding partial noncompetitive inhibitor of 20S
           proteasome activity
    • Authors: Brian B. Hasinoff; Daywin Patel
      Pages: 23 - 28
      Abstract: Publication date: 1 November 2017
      Source:Archives of Biochemistry and Biophysics, Volume 633
      Author(s): Brian B. Hasinoff, Daywin Patel
      The alcohol abuse drug disulfiram has also been shown to exhibit potent cell growth inhibitory and anticancer activity. While a number of cellular and animal studies have suggested that disulfiram exhibits its anticancer activity through interaction with the proteasome, direct evidence for inhibition of proteasome activity is lacking. In this study we show that disulfiram potently inhibits the chymotrypsin-like activity of purified human 20S proteasome at low micromolar pharmacological concentrations. The enzyme progress curves displayed characteristics of a slow-binding reaction, similar to that observed for the FDA-approved proteasomal-targeted anticancer drugs bortezomib and carfilzomib. The apparent second order rate constant for reaction with 20s proteasome that was derived from an analysis of the progress curves was about 250-fold smaller than for bortezomib and carfilzomib. The concentration dependence of the enzyme kinetics was consistent with partial noncompetitive inhibition, whereby the putative disulfiram-proteasome adduct retains, partial but decreased enzyme activity. Disulfiram, which is known to have a high affinity for protein thiols, likely reacted with a non-critical cysteine residue, and not at the proteasome substrate binding site.

      PubDate: 2017-09-09T00:00:30Z
      DOI: 10.1016/j.abb.2017.09.003
      Issue No: Vol. 633 (2017)
       
  • Bisphenol A and estrogen induce proliferation of human thyroid tumor cells
           via an estrogen-receptor-dependent pathway
    • Authors: YongHong Zhang; Feng Wei; Jing Zhang; Lanxiang Hao; Jie Jiang; Liansheng Dang; Dan Mei; ShanShan Fan; Yajin Yu; Ling Jiang
      Pages: 29 - 39
      Abstract: Publication date: 1 November 2017
      Source:Archives of Biochemistry and Biophysics, Volume 633
      Author(s): YongHong Zhang, Feng Wei, Jing Zhang, Lanxiang Hao, Jie Jiang, Liansheng Dang, Dan Mei, ShanShan Fan, Yajin Yu, Ling Jiang
      Objective To determine the relationship between papillary thyroid carcinoma and environmental exposure to bisphenol A (BPA) or 17-β estrogen (E2) by assessing the effects of these compounds on estrogen receptor expression and AKT/mTOR signaling. Methods The effects of low levels of BPA (1mM-10nM) and 17β-estradiol (E2, 0.1mM-1nM) on ER expression and cellular proliferation were determined in human thyroid papillary cancer BHP10-3 cells. Protein and mRNA levels of estrogen nuclear receptors (ERα/ERβ) and membrane receptors (GPR30) were determined by immunofluorescence assay, Western blotting, and RT-PCR, respectively, and proliferation was assessed by CCK-8 assay. Results The proliferative effects of BPA and E2 were both concentration- and time-dependent. Expression of ERα/ERβ and GPR30 were enhanced by BPA and E2. BPA and E2 could quickly phosphorylate AKT/mTOR. Moreover, ICI suppressed ERα expression and activated GPR30 as did G-1. G-15 reversed the effects of E2 on GPR30 and AKT/mTOR, but did not alter the effect of BPA. Conclusions BPA influences thyroid cancer proliferation by regulating expression of ERs and GPR30, a mechanism that differs from E2. In addition, ICI and G-15 may have the potential to be used as anti-thyroid cancer agents.

      PubDate: 2017-09-09T00:00:30Z
      DOI: 10.1016/j.abb.2017.09.002
      Issue No: Vol. 633 (2017)
       
  • The soluble domains of Gpi8 and Gaa1, two subunits of
           glycosylphosphatidylinositol transamidase (GPI-T), assemble into a complex
           
    • Authors: Dilani G. Gamage; Yug Varma; Jennifer L. Meitzler; Rachel Morissette; Travis J. Ness; Tamara L. Hendrickson
      Pages: 58 - 67
      Abstract: Publication date: 1 November 2017
      Source:Archives of Biochemistry and Biophysics, Volume 633
      Author(s): Dilani G. Gamage, Yug Varma, Jennifer L. Meitzler, Rachel Morissette, Travis J. Ness, Tamara L. Hendrickson
      Glycosylphosphatidylinositol transamidase (GPI-T) catalyzes the post-translational addition of the GPI anchor to the C-terminus of some proteins. In most eukaryotes, Gpi8, the active site subunit of GPI-T, is part of a hetero-pentameric complex containing Gpi16, Gaa1, Gpi17, and Gab1. Gpi8, Gaa1, and Gpi16 co-purify as a heterotrimer from Saccharomyces cerevisiae, suggesting that they form the core of the GPI-T. Details about the assembly and organization of these subunits have been slow to emerge. We have previously shown that the soluble domain of S. cerevisiae Gpi8 (Gpi823-306) assembles as a homodimer, similar to the caspases with which it shares weak sequence homology (Meitzler, J. L. et al., 2007). Here we present the characterization of a complex between the soluble domains of Gpi8 and Gaa1. The complex between GST-Gpi823-306 (α) and His6-Gaa150-343 (β) was characterized by native gel analysis and size exclusion chromatography (SEC) and results are most consistent with an α2β2 stoichiometry. These results demonstrate that Gpi8 and Gaa1 interact specifically without a requirement for other subunits, bring us closer to determining the stoichiometry of the core subunits of GPI-T, and lend further credence to the hypothesis that these three subunits assemble into a dimer of a trimer.
      Graphical abstract image

      PubDate: 2017-09-15T00:12:36Z
      DOI: 10.1016/j.abb.2017.09.006
      Issue No: Vol. 633 (2017)
       
  • Topoisomerase IIβ and its role in different biological contexts
    • Authors: V. Satish Bollimpelli; Pankaj S. Dholaniya; Anand K. Kondapi
      Pages: 78 - 84
      Abstract: Publication date: 1 November 2017
      Source:Archives of Biochemistry and Biophysics, Volume 633
      Author(s): V. Satish Bollimpelli, Pankaj S. Dholaniya, Anand K. Kondapi
      Topoisomerase IIβ is a type II DNA topoisomerase that was reported to be expressed in all mammalian cells but abundantly expressed in cells that have undergone terminal differentiation to attain a post mitotic state. Enzymatically it catalyzes ATP-dependent topological changes of double stranded DNA, while as a protein it was reported to be associated with several factors in promoting cell growth, migration, DNA repair and transcription regulation. The cellular roles of topoisomerase IIβ are very less understood compared to its counterpart topoisomerase IIα. This review discusses origin of Topoisomerase II beta, its structure, activities reported in vitro and in vivo along with implications in cellular processes namely transcription, DNA repair, neuronal development, aging, HIV-infection and cancer.

      PubDate: 2017-09-15T00:12:36Z
      DOI: 10.1016/j.abb.2017.06.021
      Issue No: Vol. 633 (2017)
       
  • CFTR modulates RPS27 gene expression using chloride anion as signaling
           effector
    • Authors: Ángel G. Valdivieso; Consuelo Mori; Mariángeles Clauzure; Macarena Massip-Copiz; Tomás A. Santa-Coloma
      Pages: 103 - 109
      Abstract: Publication date: Available online 21 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Ángel G. Valdivieso, Consuelo Mori, Mariángeles Clauzure, Macarena Massip-Copiz, Tomás A. Santa-Coloma
      In Cystic Fibrosis (CF), the impairment of the CFTR channel activity leads to a variety of alterations, including differential gene expression. However, the CFTR signaling mechanisms remain unclear. Recently, culturing IB3-1 CF cells under different intracellular Cl− concentrations ([Cl−]i), we observed several Cl−-dependent genes and further characterized one of them as RPS27. Thus, we hypothesized that Cl− might act as a signaling effector for CFTR signaling. Here, to test this idea, we study RPS27 expression in T84 cells modulating the CFTR activity by using CFTR inhibitors. First, we observed that incubation of T84 cells with increasing concentrations of the CFTR inhibitors CFTR(inh)-172 or GlyH-101 determined a progressive increase in the relative [Cl−]i (using the Cl− fluorescent probe SPQ). The [Cl−]i rise was concomitant with a dose-dependent down-regulation of RPS27. These results imply that CFTR inhibition produce Cl− accumulation and that RPS27 expression can be modulated by CFTR inhibition. Therefore, Cl− behaves as a signaling effector for CFTR in the modulation of RPS27 expression. In addition, the IL-1β receptor antagonist IL1RN or the JNK inhibitor SP600125, both restored the down-regulation of RPS27 induced by CFTRinh-172, implying a role of autocrine IL-1β and JNK signaling downstream of Cl− in RPS27 modulation.
      Graphical abstract image

      PubDate: 2017-09-26T19:44:48Z
      DOI: 10.1016/j.abb.2017.09.014
      Issue No: Vol. 633 (2017)
       
  • Tetramer as efficient structural mode for organizing antioxidative
           carboxylic acids: The case in inhibiting DNA oxidation
    • Authors: Ri Zhou; Zai-Qun Liu
      Pages: 1 - 10
      Abstract: Publication date: 1 October 2017
      Source:Archives of Biochemistry and Biophysics, Volume 631
      Author(s): Ri Zhou, Zai-Qun Liu
      To overcome the problem on the relationship of antioxidative effect with the branch number in a tetramer, we herein designed a series of antioxidants with pentaerythritol, glycerol, and ethylene glycol as the cores, and gallic, ferulic, caffeic, and p-hydroxybenzoic acids as the antioxidative moieties. In the case of DNA oxidation mediated by 2,2′-azobis(2-amidinopropane hydrochloride, AAPH), it was found that the stoichiometric factor (n) of a carboxylic acid increased rapidly when the acid was esterified with ethylene glycol, glycerol, and pentaerythritol to form a dimer, trimer, and tetramer, respectively. Interestingly, the coefficient in the equation of n∼{branch} ({branch} referred to the number of branches) was higher than one, indicating that the antioxidative effect was enhanced more promptly than the increase of the number of branches. Meanwhile, tetramer exhibited high intercalation effect with DNA strand. Therefore, additionally antioxidative effect was ascribed to the tethering effect resulting from tetrameric structure and strong intercalation with DNA strand generated by tetramer.
      Graphical abstract image

      PubDate: 2017-08-15T01:57:32Z
      DOI: 10.1016/j.abb.2017.08.002
      Issue No: Vol. 631 (2017)
       
  • Circadian rhythmicity: A functional connection between differentiated
           embryonic chondrocyte-1 (DEC1) and small heterodimer partner (SHP)
    • Authors: Marek M. Marczak; Bingfang Yan
      Pages: 11 - 18
      Abstract: Publication date: 1 October 2017
      Source:Archives of Biochemistry and Biophysics, Volume 631
      Author(s): Marek M. Marczak, Bingfang Yan
      Circadian rhythm misalignment has been increasingly recognized to pose health risk for a wide range of diseases, particularly metabolic disorders. The liver maintains metabolic homeostasis and expresses many circadian genes, such as differentiated embryo chondrocyte-1 (DEC1) and small heterodimer partner (SHP). DEC1 is established to repress transcription through E-box elements, and SHP belongs to the superfamily of nuclear receptors and has multiple E-box elements in its promoter. Importantly, DEC1 and SHP are inversely oscillated. This study was performed to test the hypothesis that the SHP gene is a target gene of DEC1. Cotransfection demonstrated that DEC1 repressed the SHP promoter and attenuated the transactivation of the classic circadian activator complex of Clock/Bmal1. Site-directed mutagenesis, electrophoretic mobility shift assay and chromatin immunoprecipitation established that the repression was achieved through the E-box in the proximal promoter. Transfection of DEC1 suppressed the expression of SHP. In circadian-inducing cells, the epileptic agent valproate inversely altered the expression of DEC1 and SHP. Both DEC1 and SHP are involved in energy balance and valproate is known to induce hepatic steatosis. Our findings collectively establish that DEC1 participates in the negative loop of SHP oscillating expression with potential implications in metabolic homeostasis.

      PubDate: 2017-08-15T01:57:32Z
      DOI: 10.1016/j.abb.2017.08.004
      Issue No: Vol. 631 (2017)
       
  • The novel heme-dependent inducible protein, SRRD regulates heme
           biosynthesis and circadian rhythms
    • Authors: Yuka Adachi; Mana Umeda; Asako Kawazoe; Tetsuya Sato; Yasuyuki Ohkawa; Sakihito Kitajima; Shingo Izawa; Ikuko Sagami; Shigeru Taketani
      Pages: 19 - 29
      Abstract: Publication date: 1 October 2017
      Source:Archives of Biochemistry and Biophysics, Volume 631
      Author(s): Yuka Adachi, Mana Umeda, Asako Kawazoe, Tetsuya Sato, Yasuyuki Ohkawa, Sakihito Kitajima, Shingo Izawa, Ikuko Sagami, Shigeru Taketani
      Heme plays a role in the regulation of the expression of genes related to circadian rhythms and heme metabolism. In order to identify new heme-regulated proteins, an RNA sequence analysis using mouse NIH3T3 cells treated without or with 5-aminolevulinic acid (ALA) was performed. Among the changes observed in the levels of various mRNAs including heme oxygenase-1 (HO-1) and ALA synthase-1 (ALAS1), a mouse homologue of the plant circadian-regulating protein SRR1, SRR1 domain containing (SRRD) was induced by the ALA treatment. The expression of SRRD was dependent on heme biosynthesis, and increased the production of heme. SRRD was expressed under circadian rhythms, and influenced the expression of clock genes including PER2, BMAL1, and CLOCK. The knockout of SRRD arrested the growth of cells, indicating that SRRD plays roles in heme-regulated circadian rhythms and cell proliferation.

      PubDate: 2017-08-15T01:57:32Z
      DOI: 10.1016/j.abb.2017.08.006
      Issue No: Vol. 631 (2017)
       
  • Corrigendum to “A comprehensive review on the colourless carotenoids
           phytoene and phytofluene” [Arch. Biochem. Biophys. 572 (2015) 188–200]
           
    • Authors: Antonio J. Meléndez-Martínez; Paula Mapelli-Brahm; Ana Benítez-González; Carla M. Stinco
      First page: 30
      Abstract: Publication date: 1 October 2017
      Source:Archives of Biochemistry and Biophysics, Volume 631
      Author(s): Antonio J. Meléndez-Martínez, Paula Mapelli-Brahm, Ana Benítez-González, Carla M. Stinco


      PubDate: 2017-08-25T02:59:13Z
      DOI: 10.1016/j.abb.2017.08.005
      Issue No: Vol. 631 (2017)
       
  • Thiol dioxygenase turnover yields benzothiazole products from
           2-mercaptoaniline and O2-dependent oxidation of primary alcohols
    • Authors: William P. Morrow; Sinjinee Sardar; Pawan Thapa; Mohammad S. Hossain; Frank W. Foss; Brad S. Pierce
      Pages: 66 - 74
      Abstract: Publication date: 1 October 2017
      Source:Archives of Biochemistry and Biophysics, Volume 631
      Author(s): William P. Morrow, Sinjinee Sardar, Pawan Thapa, Mohammad S. Hossain, Frank W. Foss, Brad S. Pierce
      Thiol dioxygenases are non-heme mononuclear iron enzymes that catalyze the O2-dependent oxidation of free thiols (-SH) to produce the corresponding sulfinic acid (-SO2 -). Previous chemical rescue studies identified a putative FeIII-O2 − intermediate that precedes substrate oxidation in Mus musculus cysteine dioxygenase (Mm CDO). Given that a similar reactive intermediate has been identified in the extradiol dioxygenase 2, 3-HCPD, it is conceivable that these enzymes share other mechanistic features with regard to substrate oxidation. To explore this possibility, enzymatic reactions with Mm CDO (as well as the bacterial 3-mercaptopropionic acid dioxygenase, Av MDO) were performed using a substrate analogue (2-mercaptoaniline, 2ma ). This aromatic thiol closely approximates the catecholic substrate of homoprotocatechuate of 2, 3-HPCD while maintaining the 2-carbon thiol-amine separation preferred by Mm CDO. Remarkably, both enzymes exhibit 2ma -gated O2-consumption; however, none of the expected products for thiol dioxygenase or intra/extradiol dioxygenase reactions were observed. Instead, benzothiazoles are produced by the condensation of 2ma with aldehydes formed by an off-pathway oxidation of primary alcohols added to aqueous reactions to solubilize the substrate. The observed oxidation of 1º-alcohols in 2ma -reactions is consistent with the formation of a high-valent intermediate similar to what has been reported for cytochrome P450 and mononuclear iron model complexes.
      Graphical abstract image

      PubDate: 2017-08-25T02:59:13Z
      DOI: 10.1016/j.abb.2017.08.013
      Issue No: Vol. 631 (2017)
       
  • Association between ROS production, swelling and the respirasome integrity
           in cardiac mitochondria
    • Authors: Sehwan Jang; Sabzali Javadov
      Pages: 1 - 8
      Abstract: Publication date: 15 September 2017
      Source:Archives of Biochemistry and Biophysics, Volume 630
      Author(s): Sehwan Jang, Sabzali Javadov
      Although mitochondrial Ca2+ overload and ROS production play a critical role in mitochondria-mediated cell death, a cause-effect relationship between them remains elusive. This study elucidated the crosstalk between mitochondrial swelling, ROS production, and electron transfer chain (ETC) supercomplexes in rat heart mitochondria in response to Ca2+ and tert-butyl hydroperoxide (TBH), a lipid-soluble organic peroxide. Results showed that ROS production induced by TBH was significantly increased in the presence of Ca2+ in a dose-dependent manner. TBH markedly inhibited the state 3 respiration rate with no effect on the mitochondrial swelling. Ca2+ exerted a slight effect on mitochondrial respiration that was greatly aggravated by TBH. Analysis of supercomplexes revealed a minor difference in the presence of TBH and/or Ca2+. However, incubation of mitochondria in the presence of high Ca2+ (1 mM) or inhibitors of ETC complexes (rotenone and antimycin A) induced disintegration of the main supercomplex, respirasome. Thus, PTP-dependent swelling of mitochondria solely depends on Ca2+ but not ROS. TBH has no effect on the respirasome while Ca2+ induces disintegration of the supercomplex only at a high concentration. Intactness of individual ETC complexes I and III is important for maintenance of the structural integrity of the respirasome.

      PubDate: 2017-07-26T04:45:29Z
      DOI: 10.1016/j.abb.2017.07.009
      Issue No: Vol. 630 (2017)
       
  • Low temperature plasma induces angiogenic growth factor via up-regulating
           hypoxia–inducible factor 1α in human dermal fibroblasts
    • Authors: Hui Song Cui; So Young Joo; Dae Hoon Lee; Joo Hyang Yu; Je Hoon Jeong; June-Bum Kim; Cheong Hoon Seo
      Pages: 9 - 17
      Abstract: Publication date: Available online 24 July 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Hui Song Cui, So Young Joo, Dae Hoon Lee, Joo Hyang Yu, Je Hoon Jeong, June-Bum Kim, Cheong Hoon Seo
      Numerous studies on the application of low temperature plasma (LTP) have produced impressive results, including antimicrobial, antitumor, and wound healing effects. Although LTP research has branched out to include medical applications, the detailed effects and working mechanisms of LTP on wound healing have not been fully investigated. Here, we investigated the potential effect of inducing growth factor after exposure to LTP and demonstrated the increased expression of angiogenic growth factor mediated by LTP-induced HIF1α expression in primary cultured human dermal fibroblasts. In cell viability assays, fibroblast viability was reduced 6 h and 24 h after LTP treatment for only 5 min, and pre-treating with NAC, a ROS scavenger, prevented cell loss. Fibroblast migration significantly increased at 6 h and 24 h in scratch wound healing assays, the expression of cytokines significantly changed, and regulatory growth factors were induced at 6 h and 24 h after exposure to LTP in RT-PCR or ELISAs. Specifically, LTP treatment significantly induced the expression of HIF1α, an upstream regulator of angiogenesis. Pre-treatment with the inhibitor CAY10585 abolished HIF1α expression and prevented LTP-induced angiogenic growth factor production according to immunoblotting, immunocytochemistry, and ELISA results. Taken together, our results provide information on the molecular mechanism by which LTP application may promote angiogenesis and will aid in developing methods to improve wound healing.

      PubDate: 2017-07-26T04:45:29Z
      DOI: 10.1016/j.abb.2017.07.012
      Issue No: Vol. 630 (2017)
       
  • The cardiomyopathy-associated K15N mutation in tropomyosin alters actin
           filament pointed end dynamics
    • Authors: Mert Colpan; Thu Ly; Samantha Grover; Dmitri Tolkatchev; Alla S. Kostyukova
      Pages: 18 - 26
      Abstract: Publication date: 15 September 2017
      Source:Archives of Biochemistry and Biophysics, Volume 630
      Author(s): Mert Colpan, Thu Ly, Samantha Grover, Dmitri Tolkatchev, Alla S. Kostyukova
      Correct assembly of thin filaments composed of actin and actin-binding proteins is of crucial importance for properly functioning muscle cells. Tropomyosin (Tpm) mediates the binding of tropomodulin (Tmod) and leiomodin (Lmod) at the slow-growing, or pointed, ends of the thin filaments. Together these proteins regulate thin filament lengths and actin dynamics in cardiac muscle. The K15N mutation in the TPM1 gene is associated with familial dilated cardiomyopathy (DCM) but the effect of this mutation on Tpm's function is unknown. In this study, we introduced the K15N mutation in striated muscle α-Tpm (Tpm1.1) and investigated its interaction with actin, Tmod and Lmod. The mutation caused a ∼3-fold decrease in the affinity of Tpm1.1 for actin. The binding of Lmod and Tmod to Tpm1.1-covered actin filaments also decreased in the presence of the K15N mutation. Furthermore, the K15N mutation in Tpm1.1 disrupted the inhibition of actin polymerization and affected the competition between Tmod1 and Lmod2 for binding at the pointed ends. Our data demonstrate that the K15N mutation alters pointed end dynamics by affecting molecular interactions between Tpm1.1, Lmod2 and Tmod1.

      PubDate: 2017-08-25T02:59:13Z
      DOI: 10.1016/j.abb.2017.07.006
      Issue No: Vol. 630 (2017)
       
  • l-cysteine supplementation increases insulin sensitivity mediated by
           upregulation of GSH and adiponectin in high glucose treated 3T3-L1
           adipocytes
    • Authors: Arunkumar E. Achari; Sushil K. Jain
      Pages: 54 - 65
      Abstract: Publication date: 15 September 2017
      Source:Archives of Biochemistry and Biophysics, Volume 630
      Author(s): Arunkumar E. Achari, Sushil K. Jain
      Diabetic patients have lower blood levels of l-cysteine (LC) and glutathione (GSH). This study examined the hypothesis that LC supplementation positively up regulates the effects of insulin on GSH and glucose metabolism in 3T3-L1 adipocyte model. 3T3L1 adipocytes were treated with LC (250 μM, 2 h) and/or insulin (15 or 30 nM, 2 h), and high glucose (HG, 25 mM, 20 h). Results showed that HG caused significant increase (95%) in ROS and reduction in the protein levels of DsbA-L (43%), adiponectin (64%), GCLC (20%), GCLM (21%), GSH (50%), and GLUT-4 (23%) in adipocytes. Furthermore, HG caused a reduction in total (35%) and HMW adiponectin (30%) secretion. Treatment with insulin alone significantly (p < 0.05) reduced ROS levels as well as increased DsbA-L, adiponectin, GCLC, GCLM, GSH, and GLUT-4 protein levels, glucose utilization, and improved total and HMW adiponectin secretion in HG treated adipocytes compared to HG alone. Interestingly, LC supplementation along with insulin caused greater reduction in ROS levels and significantly (p < 0.05) boosted the DsbA-L (41% vs LC, 29% vs Insulin), adiponectin (92% Vs LC, 84% Vs insulin) protein levels and total (32% Vs LC, 22% Vs insulin) and HMW adiponectin (75% Vs LC, 39% Vs insulin) secretion compared with the either insulin or LC alone in HG-treated cells. In addition, LC supplementation along with insulin increased GCLC (21% Vs LC, 14% insulin), GCLM (28% Vs LC, 16% insulin) and GSH (25% Vs LC and insulin) levels compared with the either insulin or LC alone in HG-treated cells. Furthermore, LC and insulin increases GLUT-4 protein expression (65% Vs LC, 18% Vs Insulin), glucose utilization (57% Vs LC, 27% Vs insulin) compared with the either insulin or LC alone in HG-treated cells. Similarly, LC supplementation increased insulin action significantly in cells maintained in medium contained control glucose. To explore the beneficial effect of LC is mediated by the upregulation of GCLC, we knocked down GCLC using siRNA in adipoctyes. There was a significant decrease in DsbA-L and GLUT-4 mRNA levels and GSH levels in GCLC knockdown adipocytes and LC supplementation up regulates GCLC, DsbA-L and GLUT-4 mRNA expression and GSH levels in GCLC knockdown cells. These results demonstrated that LC along with insulin increases GSH levels thereby improving adiponectin secretion and glucose utilization in adipocytes. This suggests that LC supplementation can increase insulin sensitivity and can be used as an adjuvant therapy for diabetes.

      PubDate: 2017-08-04T05:28:30Z
      DOI: 10.1016/j.abb.2017.07.016
      Issue No: Vol. 630 (2017)
       
  • Destructive effect of non-enzymatic glycation on catalase and remediation
           via curcumin
    • Authors: Fayezeh Mofidi Najjar; Fereshteh Taghavi; Rahim Ghadari; Nader Sheibani; Ali Akbar Moosavi-Movahedi
      Pages: 81 - 90
      Abstract: Publication date: 15 September 2017
      Source:Archives of Biochemistry and Biophysics, Volume 630
      Author(s): Fayezeh Mofidi Najjar, Fereshteh Taghavi, Rahim Ghadari, Nader Sheibani, Ali Akbar Moosavi-Movahedi
      Non-enzymatic glycation of proteins is a post-translational modification that is produced by a covalent binding between reducing sugars and amino groups of lysine and arginine residues. In this paper the effect of pathological conditions, derived from hyperglycemia on bovine liver catalase (BLC) as a model protein was considered by measuring enzyme activity, reactive oxygen species (ROS) generation, and changes in catalase conformational properties. We observed that in the presence of glucose, the catalase activity gradually decreased. ROS generation was also involved in the glycation process. Thus, decreased BLC activity was partly considered as a result of ROS generation through glycation. However, in the presence of curcumin the amount of ROS was reduced resulting in increased activity of the glycated catalase. The effect of high glucose level and the potential inhibitory effect of curcumin on aggregation and structural changes of catalase were also investigated. Molecular dynamic simulations also showed that interaction of catalase with curcumin resulted in changes in accessible surface area (ASA) and pKa, two effective parameters of glycation, in potential glycation lysine residues. Thus, the decrease in ASA and increase in pKa of important lysine residues were considered as predominant factors in decreased glycation of BLC by curcumin.

      PubDate: 2017-08-15T01:57:32Z
      DOI: 10.1016/j.abb.2017.06.018
      Issue No: Vol. 630 (2017)
       
  • Polydatin protects against carbon tetrachloride-induced liver fibrosis in
           mice
    • Authors: Xinyi Zhao; Rui Li; Ying Liu; Xuehong Zhang; Min Zhang; Zhi Zeng; Limin Wu; Xuelin Gao; Tian Lan; Yiqing Wang
      Pages: 1 - 7
      Abstract: Publication date: 1 September 2017
      Source:Archives of Biochemistry and Biophysics, Volume 629
      Author(s): Xinyi Zhao, Rui Li, Ying Liu, Xuehong Zhang, Min Zhang, Zhi Zeng, Limin Wu, Xuelin Gao, Tian Lan, Yiqing Wang
      Reactive oxygen species (ROS) play a key role in chronic liver injury and fibrosis. Polydatin, a glucoside of resveratrol, has been shown to possess anti-oxidative bioactivity. It has been demonstrated that resveratrol has many therapeutic effects on liver disorders including liver fibrosis. Recent study showed that polydatin prevented acute liver injury after carbon tetrachloride (CCl4) induction. However, the protective effects of polydatin on chronic liver injury and fibrosis has not been understood. Thus, we aimed to determine the roles of polydatin in chronic liver injury and fibrosis. Mice were induced by CCl4 for 6 weeks to develop chronic liver injury and fibrosis. Mice were treated with polydatin for 3 and 6 weeks, respectively. After 6 week injection of CCl4, the levels of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were markedly increased. The hepatic expression of α-SMA, collagen deposition and macrophage filtration were also increased. Furthermore, hepatic 4-HNE production and NOX4 expression were also increased in CCl4-induced mice. In contrast, polydatin ameliorated impaired liver function and histology. Moreover, polydatin attenuated liver fibrosis and inflammation in mice induced by CCl4. Additionally, polydatin suppressed hepatic 4-HNE production and NOX4 expression. In conclusion, polydatin ameliorate chronic liver injury and fibrosis through inhibition of oxidative stress and inflammation.

      PubDate: 2017-07-01T02:10:13Z
      DOI: 10.1016/j.abb.2017.06.017
      Issue No: Vol. 629 (2017)
       
  • Functional significance of C-terminal mobile domain of cardiac troponin I
    • Authors: Nazanin Bohlooli Ghashghaee; Peter O. Awinda; Bertrand C.W. Tanner; Wen-Ji Dong
      Pages: 256a - 257a
      Abstract: Publication date: Available online 27 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Nazanin Bohlooli Ghashghaee, Bertrand C.W. Tanner, Wen-Ji Dong
      Ca2+-regulation of cardiac contractility is mediated through the troponin complex, which comprises three subunits: cTnC, cTnI, and cTnT. As intracellular [Ca2+] increases, cTnI reduces its binding interactions with actin to primarily interact with cTnC, thereby enabling contraction. A portion of this regulatory switching involves the mobile domain of cTnI (cTnI-MD), the role of which in muscle contractility is still elusive. To study the functional significance of cTnI-MD, we engineered two cTnI constructs in which the MD was truncated to various extents: cTnI(1–167) and cTnI(1–193). These truncations were exchanged for endogenous cTnI in skinned rat papillary muscle fibers, and their influence on Ca2+-activated contraction and cross-bridge cycling kinetics was assessed at short (1.9 μm) and long (2.2 μm) sarcomere lengths (SLs). Our results show that the cTnI(1–167) truncation diminished the SL-induced increase in Ca2+-sensitivity of contraction, but not the SL-dependent increase in maximal tension, suggesting an uncoupling between the thin and thick filament contributions to length dependent activation. Compared to cTnI(WT), both truncations displayed greater Ca2+-sensitivity and faster cross-bridge attachment rates at both SLs. Furthermore, cTnI(1–167) slowed MgADP release rate and enhanced cross-bridge binding. Our findings imply that cTnI-MD truncations affect the blocked-to closed-state transition(s) and destabilize the closed-state position of tropomyosin.

      PubDate: 2017-10-04T03:45:58Z
      DOI: 10.1016/j.bpj.2016.11.1399
      Issue No: Vol. 112, No. 3 (2017)
       
  • Automatic regulation of NF-κB by pHSP70/IκBαm to prevent
           acute lung injury in mice
    • Abstract: Publication date: 15 November 2017
      Source:Archives of Biochemistry and Biophysics, Volume 634
      Author(s): Hai-Ying Dong, Yan Cui, Bo Zhang, Ying Luo, Yan-Xia Wang, Ming-Qing Dong, Man-Ling Liu, Peng-Tao Zhao, Wen Niu, Zhi-Chao Li
      Controlling target gene expression is a vital step in the procedure of gene therapy upon acute lung injury (ALI). Excessive activation of nuclear factor-kappa B (NF-κB) has been the key point of the inflammation overwhelming process in onset of ALI. We designed and tested a variety of plasmid named pHSP70/IκBαm which conditionally carries a mutant inhibitor of kappa B (IκB) transgene to regulate the activity of NF-κB signaling pathway in its response to an inflammatory stimulus that causes acute lung injury. Results recorded along our experiments showed that pHSP70/IκBαm was able to control mutant IκB expression in RAW264.7 cells with reference to the level of inflammatory response induced by LPS, thereby inhibiting NF-κB activation and downstream inflammatory cytokine expression. Vivo experiments revealed that construction naming pHSP70/IκBαm reduced LPS-induced lung injury and the secretion of inflammatory factors from lungs, hearts, and livers of sample mice in a LPS dose-dependent manner. In conclusion, the promoter heat shocking protein 70(HSP70) regulatory sequence of the construction was shown to drive mutant IκB expression so that its levels were positively associated with the dose of LPS used to induce acute lung injury. NF-κB activation and the downstream expression of inflammatory factors were therefore down-regulated in along an efficient path and ameliorating the damage as a consequence of LPS-induced acute lung injury.

      PubDate: 2017-10-14T08:31:24Z
       
  • GADD45 family proteins suppress JNK signaling by targeting MKK7
    • Abstract: Publication date: Available online 14 October 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Takumi Ueda, Yuri Kohama, Ayana Kuge, Eriko Kido, Hiroshi Sakurai
      Growth arrest and DNA damage-inducible 45 (GADD45) family genes encode related proteins, including GADD45α, GADD45β, and GADD45γ. In HeLa cells, expression of GADD45 members is differentially regulated under a variety of environmental conditions, but thermal and genotoxic stresses induce the expression of all genes. The heat shock response of GADD45β is mediated by the heat shock transcription factor 1 (HSF1), and GADD45β is necessary for heat stress survival. Heat and genotoxic stress-induced activation of c-Jun N-terminal kinase (JNK) is suppressed by the expression of GADD45 proteins. GADD45 proteins bind the JNK kinase mitogen-activated protein kinase kinase 7 (MKK7) and inhibit its activity, even under normal physiological conditions. Our findings indicate that GADD45 essentially suppresses the MKK7-JNK pathway and suggest that differentially expressed GADD45 family members fine-tune stress-inducible JNK activity.

      PubDate: 2017-10-14T08:31:24Z
       
  • Dielectric properties of plasma membrane: A signature for dyslipidemia in
           diabetes mellitus
    • Authors: Kakali Ghoshal; Subhadip Chakraborty Chirantan Das Sanatan Chattopadhyay Subhankar Chowdhury
      Abstract: Publication date: Available online 10 October 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Kakali Ghoshal, Subhadip Chakraborty, Chirantan Das, Sanatan Chattopadhyay, Subhankar Chowdhury, Maitree Bhattacharyya
      Dielectric properties of a living biological membrane play crucial role indicating the status of the cell in pathogenic or healthy condition. A distinct variation in membrane capacitance and impedance was observed for PBMC suspensions for diabetic and diabetic-dyslipidemic subjects compared to healthy control. Low frequency region were explicitly considered in electrical analysis to address complex membrane dielectric factors that alter the system capacitance of a PBMC suspension. Such variation was marked in size, morphology and membrane function of PBMCs for control and diseased cases. SEM and AFM studies reveal significant alteration in surface morphology of PBMCs in diseased condition. Side scatter of flow cytometry reveals complexity of PBMCs in diseased condition. Changes in size between groups were not found by SEM and forward scatter. Functional alteration in PBMCs was manifested by significant changes in cell membrane properties like Na+, K+ ATPase and Ca2+, Mg2+ ATPase activity, reduced plasma membrane fluidity and changes in intracellular Ca2+ content, which bear significant correlation in diabetic and diabetic dyslipidemic subjects. Therefore, dielectric parameters of PBMCs in diabetic-dyslipidemic challenges may led to interesting correlation opening the possibility of identifying crucial signature biomarkers.

      PubDate: 2017-10-11T08:24:40Z
       
  • Substitutions of S101 decrease proton and hydride transfers in the
           oxidation of betaine aldehyde by choline oxidase
    • Authors: Giovanni Gadda; Hongling Yuan
      Abstract: Publication date: Available online 10 October 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Giovanni Gadda, Hongling Yuan
      Choline oxidase oxidizes choline to glycine betaine, with two flavin-mediated reactions to convert the alcohol substrate to the carbon acid product. Proton abstraction from choline or hydrated betaine aldehyde in the wild-type enzyme occurs in the mixing time of the stopped-flow spectrophotometer, thereby precluding a mechanistic investigation. Mutagenesis of S101 rendered the proton transfer reaction amenable to study. Here, we have investigated the aldehyde oxidation reaction catalyzed by the mutant enzymes using steady-state and rapid kinetics with betaine aldehyde. Stopped-flow traces for the reductive half-reaction of the S101T/V/C variants were biphasic, corresponding to the reactions of proton abstraction and hydride transfer. In contrast, the S101A enzyme yielded monophasic traces like wild-type choline oxidase. The rate constants for proton transfer in the S101T/C/V variants decreased logarithmically with increasing hydrophobicity of residue 101, indicating a behavior different from that seen previously with choline for which no correlation was determined. The rate constants for hydride transfer also showed a logarithmic decrease with increasing hydrophobicity at position 101, which was similar to previous results with choline as a substrate for the enzyme. Thus, the hydrophilic character of S101 is necessary not only for efficient hydride transfer but also for the proton abstraction reaction.
      Graphical abstract image

      PubDate: 2017-10-11T08:24:40Z
       
  • STM2360 encodes a d-ornithine/d-lysine decarboxylase in Salmonella
           enterica serovar typhimurium
    • Authors: Robert Phillips; Pafe Poteh Katherine Miller Timothy Hoover
      Abstract: Publication date: Available online 9 October 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Robert S. Phillips, Pafe Poteh, Katherine A. Miller, Timothy R. Hoover
      STM2360 is a gene located in a small operon of undetermined function in Salmonella enterica serovar Typhimurium LT2. The amino acid sequence of STM2360 shows significant similarity (∼30% identity) to diaminopimelate decarboxylase (DapDC), a Fold III pyridoxal-5′-phosphate (PLP) dependent enzyme involved in l-lysine biosynthesis. We have found that the protein coded by STM2360 has a previously undocumented catalytic activity, d-ornithine/d-lysine decarboxylase (DOKDC). The reaction products, cadaverine and putrescine, respectively, were identified by NMR and mass spectrometry. The substrate specificity of DOKDC is d-Lysine > d-Ornithine. This is the first pyridoxal-5′-phosphate dependent decarboxylase identified to act on d-amino acids. STM2358, located in the same operon, has ornithine racemase activity. This suggests that the physiological substrate of the decarboxylase and the operon is ornithine. Homologs of STM2360 with high sequence identity (>80%) are found in other common enterobacteria, including species of Klebsiella, Citrobacter, Vibrio and Hafnia, as well as Clostridium in the Firmicutes, and Pseudomonas.
      Graphical abstract image

      PubDate: 2017-10-11T08:24:40Z
       
  • Characterization of the nuclear import pathway for BLM protein
    • Authors: Zhiqiang Duan; Jiafu Zhao Houqiang Haixu Xinqin Xiang Chen Jianming
      Abstract: Publication date: Available online 7 October 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Zhiqiang Duan, Jiafu Zhao, Houqiang Xu, Haixu Xu, Xinqin Ji, Xiang Chen, Jianming Xiong
      Numerous studies have shown that nuclear localization of BLM protein, a member of the RecQ helicases, mediated by nuclear localization signal (NLS) is critical for DNA recombination, replication and transcription, but the mechanism by which BLM protein is imported into the nucleus remains unknown. In this study, the nuclear import pathway for BLM was investigated. We found that nuclear import of BLM was inhibited by two dominant-negative mutants of importin β1 and NTF2/E42K, which lacks the ability to bind Ran and RanGDP, respectively, but was not inhibited by the Ran/Q69L, which is deficient in GTP hydrolysis. Further studies revealed that nuclear import of BLM was reconstituted using importin β1, RanGDP and NTF2 in digitonin-permeabilized HeLa cells. Moreover, BLM had direct binding to importin β1 through its NLS domain with the 14–16 HEAT repeats of importin β1. Furthermore, importin β1, Ran or NTF2 depletion by siRNA disrupted the accumulation of BLM protein in the nucleus. These results showed that BLM enters the nucleus via the importin β1, RanGDP and NTF2 dependent pathway, demonstrating for the first time the nuclear trafficking mechanism of a DNA helicase.
      Graphical abstract image

      PubDate: 2017-10-11T08:24:40Z
       
  • Raman spectroscopy reveals the lipid phase transition in preimplantation
           mouse embryos during freezing
    • Authors: K.A. Okotrub; S.Y. Amstislavsky N.V. Surovtsev
      Abstract: Publication date: Available online 6 October 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): K.A. Okotrub, S.Y. Amstislavsky, N.V. Surovtsev
      Although lipid phase transition is believed to be among the major damaging factors in oocytes and preimplantation embryos cryopreservation, lack of the appropriate experimental methods limits investigation of this phenomenon. Herein, we demonstrate the capabilities of Raman spectroscopy to detect lipid phase transition within the freezing preimplantation mouse embryos. We exploit the sensibility of antisymmetric CH2 Raman peak to the phase state of lipids. It is shown that during the freezing of the mouse embryos a lipid phase transition occurs at the temperatures between –7 and 0 °C. A similarity between CH2 mode temperature dependences of monounsaturated phospholipid (1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine) vesicles and the preimplantation mouse embryos is found down to cryogenic temperatures. Raman spectroscopy is considered as a method of choice to study lipid phase transition during preimplantation mammalian embryos freezing and cryopreservation.
      Graphical abstract image

      PubDate: 2017-10-11T08:24:40Z
       
  • Selenoprotein MsrB1 deficiency exacerbates acetaminophen-induced
           hepatotoxicity via increased oxidative damage
    • Authors: Ki Young Kim; Geun-Hee Kwak; Mahendra Pratap Singh; Vadim N. Gladyshev; Hwa-Young Kim
      Abstract: Publication date: Available online 3 October 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Ki Young Kim, Geun-Hee Kwak, Mahendra Pratap Singh, Vadim N. Gladyshev, Hwa-Young Kim
      Acetaminophen (APAP) overdose induces acute liver damage and failure via reactive oxygen species production and glutathione (GSH) depletion. Methionine sulfoxide reductase B1 (MsrB1) is an antioxidant selenoenzyme that specifically catalyzes the reduction of methionine R-sulfoxide residues. In this study, we used MsrB1 gene-knockout mice and primary hepatocytes to investigate the effect of MsrB1 on APAP-induced hepatotoxicity. Analyses of histological alterations and serum indicators of liver damage showed that MsrB1 −/− mice were more susceptible to APAP-induced acute liver injury than wild-type (MsrB1 +/+) mice. Consistent with the in vivo results, primary MsrB1 −/− hepatocytes displayed higher susceptibility to APAP-induced cytotoxicity than MsrB1 +/+ cells. MsrB1 deficiency increased hepatic oxidative stress after APAP challenge such as hydrogen peroxide production, lipid peroxidation, and protein oxidation levels. Additionally, basal and APAP-induced ratios of reduced-to-oxidized GSH (GSH/GSSG) were significantly lower in MsrB1 −/− than in MsrB1 +/+ livers. Nrf2 nuclear accumulation and heme oxygenase-1 expression levels after APAP challenge were lower in MsrB1 −/− than in MsrB1 +/+ livers, suggesting that MsrB1 deficiency attenuates the APAP-induced activation of Nrf2. Collectively, the results of this study suggest that selenoprotein MsrB1 plays a protective role against APAP-induced hepatotoxicity via its antioxidative function.

      PubDate: 2017-10-04T03:45:58Z
      DOI: 10.1016/j.abb.2017.09.020
       
  • Evolutionary conservation of EF-hand ΙΙ loop in aequorin: Priority of
           intensity to decay rate in bioluminescence emission
    • Authors: Mahsa Ebrahimi; Ammar Mohseni; Khosrow Khalifeh; Bijan Ranjbar; Reza H. Sajedi
      Abstract: Publication date: Available online 29 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Mahsa Ebrahimi, Ammar Mohseni, Khosrow Khalifeh, Bijan Ranjbar, Reza H. Sajedi
      As a Ca2+-regulated photoprotein, aequorin (Aeq) contains four EF-hand motifs, the second one lacks the standard sequence for Ca2+ coordination and doesn't bind to Ca2+. Here, we replaced this loop with a functional loop. According to structural studies, although the global stability of modified aequorin (4EFAeq) is higher than that of Aeq; increasing the local flexibility accompanied by internal structural rearrangements in 4EFAeq result in its penetrability to urea and acrylamide. A fast decay rate was observed for 4EFAeq. Assuming the presence of intermediate states in the luminescent reaction, this observation indicate that the loop replacement leads to the lowering of the half-life of intermediate states which results in increasing the rate of conformational switching of 4EFAeq to light emitting form. However, considerable reduction in initial luminescence intensity of 4EFAeq suggests that the number of functional complexes is reduced. Our findings demonstrate that the conformational effects of the second loop in Aeq elicit a delicate balance between local flexibility and global stability which may be considered as an important functional parameter in photoproteins. It was also concluded that evolutionary conservation of EF-hand ΙΙ in the current form is a consequence of priority of intensity to decay rate in bioluminescent organisms.

      PubDate: 2017-10-04T03:45:58Z
      DOI: 10.1016/j.abb.2017.09.018
       
  • The inhibitory effects of biomimetically designed peptides on
           α-synuclein aggregation
    • Authors: Niloofar Rezaeian; Niloofar Shirvanizadeh; Soheila Mohammadi; Maryam Nikkhah; Seyed Shahriar Arab
      Abstract: Publication date: Available online 28 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Niloofar Rezaeian, Niloofar Shirvanizadeh, Soheila Mohammadi, Maryam Nikkhah, Seyed Shahriar Arab
      Parkinson's disease is characterized by accumulation of inclusion bodies in dopaminergic neurons, where insoluble and fibrillar α-synuclein makes up the major component of these inclusion bodies. So far, several strategies have been applied in order to suppress α-synuclein aggregation and toxicity in Parkinson's disease. In the present study, a new database has been established by segmentation of all the proteins deposited in protein Data Bank. The database data base was searched for the sequences which adopt β structure and are identical or very similar to the regions of α-synuclein which are involved in aggregation. The adjacent β strands of the found sequences were chosen as the peptide inhibitors of α-synuclein aggregation. Two of the predicted peptides, namely KISVRV and GQTYVLPG, were experimentally proved to be efficient in suppressing aggregation of α-synuclein in vitro. Moreover, KISVRV exhibited the ability to disrupt oligomers of α-syn which are assumed to be the pathogenic species in Parkinson's disease.

      PubDate: 2017-10-04T03:45:58Z
      DOI: 10.1016/j.abb.2017.09.015
       
  • A fractionation approach applying chelating magnetic nanoparticles to
           characterize pericardial fluid's proteome
    • Authors: Trindade Paulo; Bastos Adelino Leite-Moreira Bruno Manadas Rita Ferreira Sofia
      Abstract: Publication date: Available online 23 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Fábio Trindade, Paulo Bastos, Adelino Leite-Moreira, Bruno Manadas, Rita Ferreira, Sofia F. Soares, Ana L. Daniel-da-Silva, Inês Falcão-Pires, Rui Vitorino
      Owing to their close proximity, pericardial fluid (PF)’s proteome may mirror the pathophysiological status of the heart. Despite this diagnosis potential, the knowledge of PF's proteome is scarce. Large amounts of albumin hamper the characterization of the least abundant proteins in PF. Aiming to expand PF's proteome and to validate the technique for future applications, we have fractionated and characterized the PF, using N-(trimethoxysilylpropyl)ethylenediamine triacetic acid (EDTA)-functionalized magnetic nanoparticles (NPs@EDTA) followed by a GeLC-MS/MS approach. Similarly to an albumin-depletion kit, NPs@EDTA-based fractionation was efficient in removing albumin. Both methods displayed comparable inter-individual variability, but NPs@EDTA outperformed the former with regard to the protein dynamic range as well as to the monitoring of biological processes. Overall, 565 proteins were identified, of which 297 (>50%) have never been assigned to PF. Moreover, owing to this method's good proteome reproducibility, affordability, rapid automation and high binding ability of NP@EDTA, it bears a great potential towards future clinical application.
      Graphical abstract image

      PubDate: 2017-09-26T19:44:48Z
       
  • All three human scavenger receptor class B proteins can bind and transport
           all three macular xanthophyll carotenoids
    • Authors: Rajalekshmy Shyam; Preejith Vachali; Aruna Gorusupudi; Kelly Nelson; Paul S. Bernstein
      Abstract: Publication date: Available online 23 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Rajalekshmy Shyam, Preejith Vachali, Aruna Gorusupudi, Kelly Nelson, Paul S. Bernstein
      Carotenoids are plant pigment molecules that are potent antioxidants. Carotenoids cannot be synthesized de novo; therefore, their dietary intake and transport to various tissues are essential to harness their health benefits. Two of the three scavenger receptor class B (SRB) proteins, SR-B1 and CD36, have been implicated as carotenoid transporters in lower species and in various tissues of higher animals. The function of the third SRB protein, SR-B2, in carotenoid transport is unknown. Using surface plasmon resonance (SPR) analyses, we have determined that all three human SRB proteins are capable of binding the macular xanthophyll carotenoids; lutein, zeaxanthin, and meso-zeaxanthin. By over-expressing human SRB proteins in cells that do not endogenously express SRBs, we have determined that lutein uptake is enhanced in the presence of LDL and is mediated by SR-B1 and CD36. SR-B1, SR-B2, and CD36 were able to take up significant amounts of zeaxanthin as well as meso-zeaxanthin, and uptake was increased in the presence of HDL. Our analyses revealed no apparent differences in protein expression profiles of SRBs in central and peripheral regions of human donor tissues, indicating that carotenoid-binding proteins rather than transporters are likely to mediate selective accumulation of carotenoids into the macula.

      PubDate: 2017-09-26T19:44:48Z
      DOI: 10.1016/j.abb.2017.09.013
       
  • DJ-1 activates autophagy in the repression of cardiac hypertrophy
    • Authors: Ruicong Xue; Jingzhou Jiang; Bin Dong; Weiping Tan; Yu Sun; Jingjing Zhao; Yili Chen; Yugang Dong; Chen Liu
      Abstract: Publication date: Available online 21 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Ruicong Xue, Jingzhou Jiang, Bin Dong, Weiping Tan, Yu Sun, Jingjing Zhao, Yili Chen, Yugang Dong, Chen Liu
      Cardiac hypertrophy is the risk factor of heart failure when the heart is confronted with pressure overload or neurohumoral stimuli. Autophagy, a conserved degradative pathway, is one of the important mechanisms involved in the regulation of cardiac hypertrophy. DJ-1 is a traditional anti-oxidative protein and emerging evidence suggested that DJ-1 might modulate autophagy. However, the regulation of autophagy by DJ-1 in the process of cardiac hypertrophy remains unknown. In our study, we firstly discovered that the expression of DJ-1declined in the process of pressure overload cardiac hypertrophy, and its alteration was parallel with the impairment of autophagy. Furthermore, we proved that DJ-1 knockout mice exhibited a more hypertrophied phenotype than wildtype mice in cardiac hypertrophy which indicated that DJ-1 is responsible for the repression of cardiac hypertrophy. Furthermore, DJ-1 knockout significantly exacerbated pulmonary edema due to cardiac hypertrophy. In the process of cardiac hypertrophy, DJ-1 knockout significantly impaired autophagy activation and enhanced mTORC1 and mTORC2 phosphorylation were found. Similarly, our in vitro study proved that DJ-1 overexpression ameliorated phenylephrine (PE)-induced cardiac hypertrophy and promoted autophagy activation. Taken together, DJ-1 might repress both pressure overload and PE-induced cardiac hypertrophy via the activation of autophagy.

      PubDate: 2017-09-26T19:44:48Z
      DOI: 10.1016/j.abb.2017.09.012
       
  • Introduction to flavoproteins: Beyond the classical paradigms
    • Authors: Pablo Sobrado; Giovanni Gadda
      Abstract: Publication date: Available online 21 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Pablo Sobrado, Giovanni Gadda


      PubDate: 2017-09-26T19:44:48Z
      DOI: 10.1016/j.abb.2017.08.016
       
  • Reaction rates of glutathione and ascorbate with alkyl radicals are too
           slow for protection against protein peroxidation in vivo
    • Authors: Thomas Nauser; Janusz M. Gebicki
      Abstract: Publication date: Available online 20 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Thomas Nauser, Janusz M. Gebicki
      Reaction kinetics of amino acid and peptide alkyl radicals with GSH and ascorbate, the two most abundant endogenous antioxidants, were investigated by pulse radiolysis. Rate constants in the order of 106 M−1s−1 were found. Alkyl radicals react at almost diffusion controlled rates and irreversibly with oxygen to form peroxyl radicals, and competition with this reaction is the benchmark for efficient repair in vivo. We consider repair of protein radicals and assume comparable rate constants for the reactions of GSH/ascorbate with peptide alkyl radicals and with alkyl radicals on a protein surface. Given physiological concentrations of oxygen, GSH and ascorbate, protein peroxyl radicals will always be a major product of protein alkyl radicals in vivo. Therefore, if they are formed by oxidative stress, protein alkyl radicals are a probable cause for biological damage.

      PubDate: 2017-09-20T19:20:05Z
      DOI: 10.1016/j.abb.2017.09.011
       
  • Retinol saturase modulates lipid metabolism and the production of reactive
           oxygen species
    • Authors: Xiao-Yan Pang; Suya Wang; Michael J. Jurczak; Gerald I. Shulman; Alexander R. Moise
      Abstract: Publication date: Available online 18 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Xiao-Yan Pang, Suya Wang, Michael J. Jurczak, Gerald I. Shulman, Alexander R. Moise
      Retinol saturase (RetSat) catalyzes the saturation of double bonds of all-trans-retinol leading to the production of dihydroretinoid metabolites. Beside its role in retinoid metabolism, there is evidence that RetSat modulates the cellular response to oxidative stress and plays critical roles in adipogenesis and the accumulation of lipids. Here, we explore the relationship between RetSat, lipid metabolism and oxidative stress using in vitro and in vivo models with altered expression of RetSat. Our results reveal that RetSat is a potent modulator of the cellular response to oxidative stress and the generation of reactive oxygen species (ROS). The levels of reactive aldehydes products of lipid peroxidation, as measured based on thiobarbituric acid reactivity, are increased in RetSat overexpressing cells and, conversely, reduced in cells and tissues with reduced or absent expression of RetSat compared to controls. Despite increased weight gain, neutral lipid accumulation and alterations in hepatic lipid composition, RetSat −/- mice exhibit normal responses to insulin. In conclusion, our findings further expand upon the role of RetSat in oxidative stress and lipid metabolism and could provide insight in the significance of alterations of RetSat expression as observed in metabolic disorders.

      PubDate: 2017-09-20T19:20:05Z
      DOI: 10.1016/j.abb.2017.09.009
       
  • ADP-dependent phosphofructokinases from the archaeal order
           Methanosarcinales display redundant glucokinase activity
    • Authors: Ricardo A. Zamora; Felipe Gonzalez-Órdenes; Victor Castro-Fernández; Victoria Guixé
      Abstract: Publication date: Available online 14 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Ricardo A. Zamora, Felipe Gonzalez-Órdenes, Victor Castro-Fernández, Victoria Guixé
      The genome of Methanosarcinales organisms presents both ADP-dependent glucokinase and phosphofructokinase genes. However, Methanococcoides burtonii has a truncate glucokinase gene with a large deletion at the C-terminal, where the catalytic GXGD motif is located. Characterization of its phosphofructokinase annotated protein shows that is a bifunctional enzyme able to supply the absence of the glucokinase activity. Moreover, kinetic analyses of the phosphofructokinase annotated enzyme from, Methanohalobium evestigatum demonstrated that this enzyme is also bifunctional. The high conservation of the active site residues of all the enzymes from the order Methanosarcinales suggest that they should be bifunctional, as was previously reported for the ADP-dependent kinases from Methanococcales, highlighting the redundancy of the glucokinase activity in this archaeal group. The presence of active glycolytic enzymes would be important when glycogen storage of these organisms needs to be degraded to be used as energy source. Kinetic and structural information allows us to establish a substrate specificity signature that identifies specific GK or PFK, and bifunctional enzymes in this family.

      PubDate: 2017-09-15T00:12:36Z
      DOI: 10.1016/j.abb.2017.09.008
       
  • ATP alters protein folding and function of Escherichia coli uridine
           phosphorylase
    • Authors: Yi-Kai Liu; Tzu-Hsuan Lin; Pei-Fen Liu
      Abstract: Publication date: Available online 13 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Yi-Kai Liu, Tzu-Hsuan Lin, Pei-Fen Liu
      Uridine phosphorylase is one of the critical enzymes in the pyrimidine salvage pathway. Cells regenerate uridine for nucleotide metabolism by incorporating uracil with ribose-1-phosphate with this enzyme. Recent studies indicate that Escherichia coli uridine phosphorylase is destabilized in the presence of ATP. However, the mechanism underlying the destabilization process and its influence on uridine phosphorylase function remain to be established. Here, we comprehensively investigated the effects of ATP on protein folding and function of Escherichia coli uridine phosphorylase. Our results demonstrate that ATP apparently decreases the stability of uridine phosphorylase in a concentration-dependent manner. Additionally, simply increasing the level of ATP led to a reduction of enzymatic activity to complete inhibition. Further studies showed that uridine phosphorylase accumulates as a partially unfolded state in the presence of ATP. Moreover, ATP specifically accelerated the unfolding rate of uridine phosphorylase with no observable effects on the refolding process. Our preliminary findings suggest that ATP can alter the protein folding and function of enzymes via apparent destabilization. This mechanism may be significant for proteins functioning under conditions of high levels of ATP, such as cancer cell environments.

      PubDate: 2017-09-15T00:12:36Z
      DOI: 10.1016/j.abb.2017.09.007
       
  • Non-thermal plasma induces mitochondria-mediated apoptotic signaling
           pathway via ROS generation in HeLa cells
    • Authors: Wei Li; K.N. Yu; Jie Ma; Jie Shen; Cheng Cheng; Fangjian Zhou; Zhiming Cai; Wei Han
      Abstract: Publication date: Available online 9 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Wei Li, K.N. Yu, Jie Ma, Jie Shen, Cheng Cheng, Fangjian Zhou, Zhiming Cai, Wei Han
      Non-thermal plasma (NTP) has been proposed as a novel therapeutic method for anticancer treatment. Although increasing evidence suggests that NTP selectively induces apoptosis in some types of tumor cells, the molecular mechanisms underlying this phenomenon remain unclear. In this study, we further investigated possible molecular mechanisms for NTP-induced apoptosis of HeLa cells. The results showed that NTP exposure significantly inhibited the growth and viability of HeLa cells. Morphological observation and flow cytometry analysis demonstrated that NTP exposure induced HeLa cell apoptosis. NTP exposure also activated caspase-9 and caspase-3, which subsequently cleaved poly (ADP- ribose) polymerase. Furthermore, NTP exposure suppressed Bcl-2 expression, enhanced Bax expression and translocation to mitochondria, activated mitochondria-mediated apoptotic pathway, followed by the release of cytochrome c. Further studies showed that NTP treatment led to ROS generation, whereas blockade of ROS generation by N-acetyl-l-cysteine (NAC, ROS scavengers) significantly prevented NTP-induced mitochondrial alteration and subsequent apoptosis of HeLa cells via suppressing Bax translocation, cytochrome c and caspase-3 activation. Taken together, our results indicated that NTP exposure induced mitochondria-mediated intrinsic apoptosis of HeLa cells was activated by ROS generation. These findings provide insights to the therapeutic potential and clinical research of NTP as a novel tool in cervical cancer treatment.
      Graphical abstract image

      PubDate: 2017-09-15T00:12:36Z
      DOI: 10.1016/j.abb.2017.09.005
       
  • Interplay of mitochondria apoptosis regulatory factors and microRNAs in
           valvular heart disease
    • Authors: Muhammad Ishtiaq Jan; Riaz Anwar Khan; Tahir Ali; Muhammad Bilal; Long Bo; Abdul Sajid; Abdul Malik; Naseeb Urehman; Nayyar Waseem; Javed Nawab; Murad Ali; Abdul Majeed; Hamid Ahmad; Sohail Aslam; Sadia Hamera; Aneesa Sultan; Mariam Anees; Qamar Javed; Iram Murtaza
      Abstract: Publication date: Available online 6 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Muhammad Ishtiaq Jan, Riaz Anwar Khan, Tahir Ali, Muhammad Bilal, Long Bo, Abdul Sajid, Abdul Malik, Naseeb Urehman, Nayyar Waseem, Javed Nawab, Murad Ali, Abdul Majeed, Hamid Ahmad, Sohail Aslam, Sadia Hamera, Aneesa Sultan, Mariam Anees, Qamar Javed, Iram Murtaza
      Valvular heart disease (VHD) is an active process involving a wide range of pathological changes. The major complications of VHD are stenosis and regurgitation, which are macroscopic phenomena, induced in part through cellular changes. Altered expression of mitochondria associated genes causes membrane potential depolarization, leading to the increased levels of apoptosis observed in cardiac dysfunction. Objective of this study is to find molecular medicine candidates that can control expression of the key mitochondria apoptosis regulatory genes. Present study aims to assess the way microRNA are involved in regulating mitochondrial apoptosis regulatory genes and observation of their expression in the heart valve dysfunction. Apoptotic genes PUMA and DRP1 were found to be highly expressed, whereas anti-apoptotic gene ARC was down regulated. The expression level of GATA-4 transcription factor was also reduced in cardiac valve tissues. MicroRNAs miR-15a and miR-29a were repressed, while miR-214 was up regulated. Furthermore, study showed that PUMA, DRP1 and ARC expression might be attenuated by their respective miRNAs. Our results indicate that mitochondria regulatory genes might be controlled by miR-15a, miR-29a and miR-214, in VHD patients. Present study may provide platform for future research regarding potential therapeutic role of miRNAs in CVDs.

      PubDate: 2017-09-09T00:00:30Z
      DOI: 10.1016/j.abb.2017.09.001
       
  • The catalytic activity of a recombinant single chain variable fragment
           nucleic acid-hydrolysing antibody varies with fusion tag and expression
           host
    • Authors: Joungmin Lee; Minjae Kim; Youngsil Seo; Yeonjin Lee; Hyunjoon Park; Sung June Byun; Myung-Hee Kwon
      Abstract: Publication date: Available online 6 September 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Joungmin Lee, Minjae Kim, Youngsil Seo, Yeonjin Lee, Hyunjoon Park, Sung June Byun, Myung-Hee Kwon
      The antigen-binding properties of single chain Fv antibodies (scFvs) can vary depending on the position and type of fusion tag used, as well as the host cells used for expression. The issue is even more complicated with a catalytic scFv antibody that binds and hydrolyses a specific antigen. Herein, we investigated the antigen-binding and -hydrolysing activities of the catalytic anti-nucleic acid antibody 3D8 scFv expressed in Escherichia coli or HEK293f cells with or without additional amino acid residues at the N- and C-termini. DNA-binding activity was retained in all recombinant forms. However, the DNA-hydrolysing activity varied drastically between forms. The DNA-hydrolysing activity of E. coli-derived 3D8 scFvs was not affected by the presence of a C-terminal human influenza haemagglutinin (HA) or His tag. By contrast, the activity of HEK293f-derived 3D8 scFvs was completely lost when additional residues were included at the N-terminus and/or when a His tag was incorporated at the C-terminus, whereas a HA tag at the C-terminus did not diminish activity. Thus, we demonstrate that the antigen-binding and catalytic activities of a catalytic antibody can be separately affected by the presence of additional residues at the N- and C-termini, and by the host cell type.

      PubDate: 2017-09-09T00:00:30Z
      DOI: 10.1016/j.abb.2017.09.004
       
  • Effect of conservative mutations (L94V and L94I) on the structure and
           stability of horse cytochrome c
    • Authors: Sabab Hasan Khan; Asimul Islam; Md. Imtaiyaz Hassan; Sujata Sharma; Tej Pal Singh; Faizan Ahmad
      Abstract: Publication date: Available online 26 August 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Sabab Hasan Khan, Asimul Islam, Md. Imtaiyaz Hassan, Sujata Sharma, Tej Pal Singh, Faizan Ahmad
      A sequence alignment of horse cytochrome c (cyt c) with all known cyts c shows that Leu at position 94 is conserved, except in 14 species which have either Val or Ile at this position. It is also known that Leu94 of the mammalian cyt c plays an important role in folding and stability. The important question here is as to what will happen in terms of folding and stability if Leu94 of the mammalian cyt c is substituted by Val or Ile. To answer this question, we introduced natural substitutes of Leu94 by Val and Ile in horse cyt c. The purified L94V and L94I mutants under native condition (pH 6.0, 25 °C) were characterized using far-UV, near-UV and Soret- circular dichroism, visible absorbance, Trp and ANS (1-anilino-8-napthaline sulphonate) fluorescence and dynamic light scattering measurements. Furthermore, stability parameters T m (mid-point of denaturation) and ΔG D 0 (Gibbs free energy change at 25 °C) were also determined using spectroscopic and differential scanning calorimetric methods. All these measurements led us to conclude that both mutants exist as molten globule and are less stable than the wild-type protein. These observations are supported well by examining the structure of horse cyt c (PDB ID, 1HRC).

      PubDate: 2017-09-04T04:00:59Z
      DOI: 10.1016/j.abb.2017.08.015
       
  • Role of ADP ribosylation factor6− Cytohesin1−PhospholipaseD signaling
           axis in U46619 induced activation of NADPH oxidase in pulmonary artery
           smooth muscle cell membrane
    • Authors: Sajal Chakraborti; Jaganmay Sarkar; Animesh Chowdhury; Tapati Chakraborti
      Abstract: Publication date: Available online 16 August 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Sajal Chakraborti, Jaganmay Sarkar, Animesh Chowdhury, Tapati Chakraborti
      Treatment of human pulmonary artery smooth muscle cells (HPASMCs) with the thromboxane A2 receptor antagonist, SQ29548 inhibited U46619 stimulation of phospholipase D (PLD) and NADPH oxidase activities in the cell membrane. Pretreatment with apocynin inhibited U46619 induced increase in NADPH oxidase activity. The cell membrane contains predominantly PLD2 along with PLD1 isoforms of PLD. Pretreatment with pharmacological and genetic inhibitors of PLD2, but not PLD1, attenuated U46619 stimulation of NADPH oxidase activity. U46619 stimulation of PLD and NADPH oxidase activities were insensitive to BFA and Clostridium botulinum C3 toxin; however, pretreatment with secinH3 inhibited U46619 induced increase in PLD and NADPH oxidase activities suggesting a major role of cytohesin in U46619-induced increase in PLD and NADPH oxidase activities. Arf-1, Arf-6, cytohesin-1 and cytohesin-2 were observed in the cytosolic fraction, but only Arf-6 and cytohesin-1 were translocated to the cell membrane upon treatment with U46619. Coimmunoprecipitation study showed association of Arf-6 with cytohesin-1 in the cell membrane fraction. In vitro binding of GTPγS with Arf-6 required the presence of cytohesin-1 and that occurs in BFA insensitive manner. Overall, BFA insensitive Arf6−cytohesin1 signaling axis plays a pivotal role in U46619-mediated activation of PLD leading to stimulation of NADPH oxidase activity in HPASMCs.

      PubDate: 2017-08-25T02:59:13Z
      DOI: 10.1016/j.abb.2017.08.012
       
  • Identification and quantification and antioxidant activity of flavonoids
           in different strains of silk cocoon, Bombyx mori
    • Authors: Supamas Napavichayanun; Oliver Lutz; Martin Fischnaller; Thomas Jakschitz; Günther Bonn; Pornanong Aramwit
      Abstract: Publication date: Available online 12 August 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Supamas Napavichayanun, Oliver Lutz, Martin Fischnaller, Thomas Jakschitz, Günther Bonn, Pornanong Aramwit
      Silk cocoon is produced from silkworm (Bombyx mori) to protect itself from outer environment. Various strains of cocoon contain different forms and amounts of flavonoids, which may affect on their antioxidant activity. Moreover, the extraction method would influence the amount of flavonoids extracted. Therefore, the objectives of this study were to identify and quantify the flavonoids in 3 strains of bivoltine Bombyx mori silk cocoon (Chul 1/1; white cocoon, Chul 3/2; greenish cocoon, and Chul 4/2; yellow cocoon) extracted by 6 different solvents including acetone, ethyl acetate, dimethyl sulfoxide (DMSO), ethanol, methanol, and purified water. The flavonoids extracted were identified and quantified by liquid chromatography–mass spectrometry (LC-MS). The antioxidant activity of flavonoids extracted was also investigated by visible spectroscopy at 517 nm. The results showed that Chul 3/2 silk cocoon contained the highest amount of flavonoids. Purified water seemed to be the best solvent that preserved most antioxidant activity of the flavonoids extracted. Flavonoids in Chul 1/1 and Chul 4/2 silk cocoon were rarely found, however they contained some antioxidant activities. The data from this study can provide basic information for flavonoid extraction from silk cocoon which can also apply for other flavonoid-containing natural biomaterials.

      PubDate: 2017-08-15T01:57:32Z
      DOI: 10.1016/j.abb.2017.08.010
       
  • Methionine sulfoxide reductase A protects against
           lipopolysaccharide-induced septic shock via negative regulation of the
           proinflammatory responses
    • Authors: Mahendra Pratap Singh; Ki Young Kim; Geun-Hee Kwak; Suk-Hwan Baek; Hwa-Young Kim
      Abstract: Publication date: Available online 10 August 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Mahendra Pratap Singh, Ki Young Kim, Geun-Hee Kwak, Suk-Hwan Baek, Hwa-Young Kim
      Methionine sulfoxide reductase A (MsrA) is a major antioxidant enzyme that specifically catalyzes the reduction of methionine S-sulfoxide. In this study, we used MsrA gene-knockout (MsrA –/–) mice and bone marrow-derived macrophages (BMDMs) to investigate the role of MsrA in the regulation of inflammatory responses induced by lipopolysaccharide (LPS). MsrA –/– mice were more susceptible to LPS-induced lethal shock than wild-type (MsrA +/+) mice. Serum levels of the proinflammatory cytokines IL-6 and TNF-α induced by LPS were higher in MsrA –/– than in MsrA +/+ mice. MsrA deficiency in the BMDMs also increased the LPS-induced cytotoxicity as well as TNF-α level. Basal and LPS-induced ROS levels were higher in MsrA –/– than in MsrA +/+ BMDMs. Phosphorylation levels of p38, JNK, and ERK were higher in MsrA –/– than in MsrA +/+ BMDMs in response to LPS, suggesting that MsrA deficiency increases MAPK activation. Furthermore, MsrA deficiency increased the expression and nuclear translocation of NF-κB and the expression of inducible nitric oxide synthase, a target gene of NF-κB, in response to LPS. Taken together, our results suggest that MsrA protects against LPS-induced septic shock, and negatively regulates proinflammatory responses via inhibition of the ROS–MAPK–NF-κB signaling pathways.

      PubDate: 2017-08-15T01:57:32Z
      DOI: 10.1016/j.abb.2017.08.008
       
  • Nuclear factor (erythroid-derived 2)-like 2 (NRF2) drug discovery:
           Biochemical toolbox to develop NRF2 activators by reversible binding of
           Kelch-like ECH-associated protein 1 (KEAP1)
    • Authors: Alberto Bresciani; Antonino Missineo; Mariana Gallo; Mauro Cerretani; Paola Fezzardi; Licia Tomei; Daniel Oscar Cicero; Sergio Altamura; Alessia Santoprete; Raffaele Ingenito; Elisabetta Bianchi; Robert Pacifici; Celia Dominguez; Ignacio Munoz-Sanjuan; Steven Harper; Leticia Toledo-Sherman; Larry C. Park
      Abstract: Publication date: Available online 8 August 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Alberto Bresciani, Antonino Missineo, Mariana Gallo, Mauro Cerretani, Paola Fezzardi, Licia Tomei, Daniel Oscar Cicero, Sergio Altamura, Alessia Santoprete, Raffaele Ingenito, Elisabetta Bianchi, Robert Pacifici, Celia Dominguez, Ignacio Munoz-Sanjuan, Steven Harper, Leticia Toledo-Sherman, Larry C. Park
      Mechanisms that activate innate antioxidant responses, as a way to mitigate oxidative stress at the site of action, hold much therapeutic potential in diseases, such as Parkinson's disease, Alzheimer's disease and Huntington's disease, where the use of antioxidants as monotherapy has not yielded positive results. The nuclear factor NRF2 is a transcription factor whose activity upregulates the expression of cell detoxifying enzymes in response to oxidative stress. NRF2 levels are modulated by KEAP1, a sensor of oxidative stress. KEAP1 binds NRF2 and facilitates its ubiquitination and subsequent degradation. Recently, compounds that reversibly disrupt the NRF2-KEAP1 interaction have been described, opening the field to a new era of safer NRF2 activators. This paper describes a set of new, robust and informative biochemical assays that enable the selection and optimization of non-covalent KEAP1 binders. These include a time-resolved fluorescence resonance energy transfer (TR-FRET) primary assay with high modularity and robustness, a surface plasmon resonance (SPR) based KEAP1 direct binding assay that enables the quantification and analysis of full kinetic binding parameters and finally a 1H-15N heteronuclear single quantum coherence (HSQC) NMR assay suited to study the interaction surface of KEAP1 with residue-specific information to validate the interaction of ligands in the KEAP1 binding site.

      PubDate: 2017-08-15T01:57:32Z
      DOI: 10.1016/j.abb.2017.08.003
       
  • 2-methoxyethylacrylate modified polysulfone membrane and its blood
           compatibility
    • Authors: Xin Tian; Yun-Ren Qiu
      Abstract: Publication date: Available online 29 July 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Xin Tian, Yun-Ren Qiu
      Hydrophilic material of 2-methoxyethylacrylate (MEA) was grafted from polysulfone (PSF) membrane via Michael addition reaction. The 1H-nuclear magnetic resonance (1H NMR) and X-ray photoelectron spectroscopy (XPS) characterizations of the modified membrane showed that MEA had been successfully grafted onto PSF membrane surface. The water contact angle of the membrane surface was tested. The results showed that the water contact angle changed from 76° to 59.5°, it means that the hydrophilicity of the modified membrane was improved. A series of blood compatibility tests include bovine serum protein adsorption, platelet adhesion, prothrombin time (PT), partial thromboplastin time (APTT) and thrombin time (TT) were carried out on PSF membrane and the modified PSF membrane with highest grafted density of MEA. All of the results show that MEA plays an important role in improving the blood compatibility of PSF membrane.
      Graphical abstract image

      PubDate: 2017-08-04T05:28:30Z
      DOI: 10.1016/j.abb.2017.07.018
       
  • Human and Plasmodium serine hydroxymethyltransferases differ in
           rate-limiting steps and pH-dependent substrate inhibition behavior
    • Authors: Watcharee Amornwatcharapong; Somchart Maenpuen; Penchit Chitnumsub; Ubolsree Leartsakulpanich; Pimchai Chaiyen
      Abstract: Publication date: Available online 29 July 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Watcharee Amornwatcharapong, Somchart Maenpuen, Penchit Chitnumsub, Ubolsree Leartsakulpanich, Pimchai Chaiyen
      Serine hydroxymethyltransferase (SHMT), an essential enzyme for cell growth and development, catalyzes the transfer of -CH2OH from l-serine to tetrahydrofolate (THF) to form glycine and 5,10-methylenetetrahydrofolate (MTHF) which is used for nucleotide synthesis. Insights into the ligand binding and inhibition properties of human cytosolic SHMT (hcSHMT) and Plasmodium SHMT (PvSHMT) are crucial for designing specific drugs against malaria and cancer. The results presented here revealed strong and pH-dependent THF inhibition of hcSHMT. In contrast, in PvSHMT, THF inhibition and the influence of pH were not as pronounced. Ligand binding experiments performed at various pH values indicated that the hcSHMT:Gly complex binds THF more tightly at lower pH conditions, while the binding affinity of the PvSHMT:Gly complex for THF is not pH-dependent. Pre-steady state kinetic (rapid-quench) analysis of hcSHMT showed burst kinetics, indicating that glycine formation occurs fastest in the first turnover relative to the subsequent turnovers i.e. glycine release is the rate-limiting step in the hcSHMT reaction. All data suggest that excess THF likely binds E:Gly binary complex and forms the E:Gly:THF dead-end complex before glycine is released. A unique flap motif found in the structure of hcSHMT may be the key structural feature that imparts these described characteristics of hcSHMT.

      PubDate: 2017-08-04T05:28:30Z
      DOI: 10.1016/j.abb.2017.07.017
       
  • Crystal structure of Pisum arvense seed lectin (PAL) and characterization
           of its interaction with carbohydrates by molecular docking and dynamics
    • Authors: Vanir Reis Pinto-Junior; Mayara Queiroz Santiago; Camila Bezerra Nobre; Vinicius Jose Silva Osterne; Rodrigo Bainy Leal; Joao Batista Cajazeiras; Claudia Figueiredo Lossio; Bruno Anderson Matias Rocha; Maria Gleiciane Queiroz Martins; Clareane Avelino Simplicio Nobre; Mayara Torquato Lima Silva; Kyria Santiago Nascimento; Benildo Sousa Cavada
      Abstract: Publication date: Available online 25 July 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Vanir Reis Pinto-Junior, Mayara Queiroz Santiago, Camila Bezerra Nobre, Vinicius Jose Silva Osterne, Rodrigo Bainy Leal, Joao Batista Cajazeiras, Claudia Figueiredo Lossio, Bruno Anderson Matias Rocha, Maria Gleiciane Queiroz Martins, Clareane Avelino Simplicio Nobre, Mayara Torquato Lima Silva, Kyria Santiago Nascimento, Benildo Sousa Cavada
      The Pisum arvense lectin (PAL), a legume protein belonging to the Vicieae tribe, is capable of specific recognition of mannose, glucose and its derivatives without altering its structure. In this work, the three-dimensional structure of PAL was determined by X-ray crystallography and studied in detail by a combination of molecular docking and molecular dynamics (MD). Crystals belonging to monoclinic space group P21 were grown by the vapor diffusion method at 293 K. The structure was solved at 2.16 Å and was similar to that of other Vicieae lectins. The structure presented Rfactor and Rfree of 17.04% and 22.08%, respectively, with all acceptable geometric parameters. Molecular docking was performed to analyze interactions of the lectin with monosaccharides, disaccharides and high-mannose N-glycans. PAL demonstrated different affinities on carbohydrates, depending on bond orientation and glycosidic linkage present in ligands. Furthermore, the lectin interacted with representative N-glycans in a manner consistent with the biological effects described for Vicieae lectins. Carbohydrate-recognition domain (CRD) in-depth analysis was performed by MD, describing the behavior of CRD residues in complex with ligand, stability, flexibility of the protein over time, CRD volume and topology. This is a first report of its kind for a lectin of the Vicieae tribe.
      Graphical abstract image

      PubDate: 2017-07-26T04:45:29Z
      DOI: 10.1016/j.abb.2017.07.013
       
  • Characterization of secondary structure and lipid binding behavior of
           N-terminal saposin like subdomain of human Wnt3a
    • Authors: Aparna Krishnamoorthy; Andrzej Witkowski; Jesse J. Tran; Paul M.M. Weers; Robert O. Ryan
      Abstract: Publication date: Available online 25 July 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Aparna Krishnamoorthy, Andrzej Witkowski, Jesse J. Tran, Paul M.M. Weers, Robert O. Ryan
      Wnt signaling is essential for embryonic development and adult homeostasis in multicellular organisms. A conserved feature among Wnt family proteins is the presence of two structural domains. Within the N-terminal (NT) domain there exists a motif that is superimposable upon saposin-like protein (SAPLIP) family members. SAPLIPs are found in plants, microbes and animals and possess lipid surface seeking activity. To investigate the function of the Wnt3a saposin-like subdomain (SLD), recombinant SLD was studied in isolation. Bacterial expression of this Wnt fragment was achieved only when the core SLD included 82 NT residues of Wnt3a (NT-SLD). Unlike SAPLIPs, NT-SLD required the presence of detergent to achieve solubility at neutral pH. Deletion of two hairpin loop extensions present in NT-SLD, but not other SAPLIPs, had no effect on the solubility properties of NT-SLD. Far UV circular dichroism spectroscopy of NT-SLD yielded 50–60% α-helix secondary structure. Limited proteolysis of isolated NT-SLD in buffer and detergent micelles showed no differences in cleavage kinetics. Unlike prototypical saposins, NT-SLD exhibited weak membrane-binding affinity and lacked cell lytic activity. In cell-based canonical Wnt signaling assays, NT-SLD was unable to induce stabilization of β-catenin or modulate the extent of β-catenin stabilization induced by full-length Wnt3a. Taken together, the results indicate neighboring structural elements within full-length Wnt3a affect SLD conformational stability. Moreover, SLD function(s) in Wnt proteins appear to have evolved away from those commonly attributed to SAPLIP family members.
      Graphical abstract image

      PubDate: 2017-07-26T04:45:29Z
      DOI: 10.1016/j.abb.2017.07.015
       
  • MiR-143 regulates the proliferation and migration of osteosarcoma cells
           through targeting MAPK7
    • Authors: Xiancheng Dong; Bin Lv; Wei Liu; Qinghua Cheng; Chuan Su; Guoyong Yin
      Abstract: Publication date: Available online 20 July 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Xiancheng Dong, Bin Lv, Wei Liu, Qinghua Cheng, Chuan Su, Guoyong Yin
      Accumulating documents have been suggested that microRNA-143 (miR-143) function as a tumor suppressor, involved in many biological processes including tumor initiation and progression. However, the biological function and molecular mechanism of miR-143 in Osteosarcoma (OS) still remains to be further investigated. Despite many efforts have been made, the prognosis of OS is still unsatisfied. Thus, exploring the underlying mechanism of OS and finding new treatment targets is essential for improving the survival rate of OS patients. In our study, we determined the level of miR-143 in clinical OS tissues and cells, and explored its function and underlying mechanisms in the tumorigenesis of OS. Our findings revealed that miR-143 expression was significantly downregulated in OS tissues and cell lines. Gain-of-function assays indicated that forced expression of miR-143 in OS cells inhibited cell proliferation and migration/invasion. Bioinformatics and luciferase reporter assays confirmed that MAPK7 was targets gene of miR-143. The results of the present study indicated that miR-143 could be a potential target for treating OS.

      PubDate: 2017-07-26T04:45:29Z
      DOI: 10.1016/j.abb.2017.07.011
       
  • Interconversion of inactive to active conformation of MARK2: Insights from
           molecular modeling and molecular dynamics simulation
    • Authors: Sajjad Ahrari; Navid Mogharrab; Leila Navapour
      Abstract: Publication date: Available online 12 July 2017
      Source:Archives of Biochemistry and Biophysics
      Author(s): Sajjad Ahrari, Navid Mogharrab, Leila Navapour
      The Ser/Thr protein kinase MARK2, also known as Par1b, belongs to a highly-conserved group of PAR proteins which regulate cell polarity and partitioning through the animal kingdom. In the current study, inactive and active structures of human MARK2 were constructed by modeling and molecular dynamics simulation, based on available incomplete crystal structures in Protein Data Bank, to investigate local structural changes through which MARK2 switches from inactive to active state. None of the MARK2 wild type inactive crystal structures represent the position of activation segment. So, the contribution of this loop to the formation of inactive state is not clear. In the modeled structure of inactive MARK2, the activation segment occludes the enzyme active site and assumes a relatively stable position. We also presented a detailed description of the major structural changes occur through the activation process and proposed a framework on how these deviations might be affected by the phosphorylation of Thr208 or existence of the UBA domain. Inspection of protein active state in the presence of Mg-ATP, demonstrated the precise arrangement of the various parts of enzyme around Mg-ATP and the importance of their stability in localization of the resulting complex. The results also confirmed the alleged mild auto-inhibitory role of the UBA domain and suggested a reason for the necessity of this role, based on structural similarities to other related kinases.
      Graphical abstract image

      PubDate: 2017-07-19T03:35:38Z
      DOI: 10.1016/j.abb.2017.07.002
       
 
 
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