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  Subjects -> BIOLOGY (Total: 2958 journals)
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BIOCHEMISTRY (230 journals)                  1 2     

Showing 1 - 0 of 0 Journals sorted alphabetically
AAPS PharmSciTech     Hybrid Journal   (Followers: 6)
Acetic Acid Bacteria     Open Access   (Followers: 1)
ACS Central Science     Open Access   (Followers: 5)
ACS Chemical Biology     Full-text available via subscription   (Followers: 193)
ACS Chemical Neuroscience     Full-text available via subscription   (Followers: 15)
Acta Crystallographica Section D : Biological Crystallography     Hybrid Journal   (Followers: 10)
Acta Crystallographica Section F: Structural Biology Communications     Hybrid Journal   (Followers: 7)
Advances and Applications in Bioinformatics and Chemistry     Open Access   (Followers: 9)
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: 7)
Advances in Protein Chemistry and Structural Biology     Full-text available via subscription   (Followers: 16)
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: 7)
American Journal of Biochemistry and Biotechnology     Open Access   (Followers: 63)
American Journal of Biochemistry and Molecular Biology     Open Access   (Followers: 13)
American Journal of Polymer Science     Open Access   (Followers: 23)
Amino Acids     Hybrid Journal   (Followers: 8)
Analytical Biochemistry     Hybrid Journal   (Followers: 143)
Angiogenesis     Hybrid Journal   (Followers: 3)
Annals of Clinical Biochemistry     Hybrid Journal   (Followers: 8)
Annual Review of Biochemistry     Full-text available via subscription   (Followers: 52)
Annual Review of Chemical and Biomolecular Engineering     Full-text available via subscription   (Followers: 10)
Applied Biochemistry and Biotechnology     Hybrid Journal   (Followers: 45)
Applied Biochemistry and Microbiology     Hybrid Journal   (Followers: 17)
Applied Organometallic Chemistry     Hybrid Journal   (Followers: 5)
Archives of Biochemistry and Biophysics     Hybrid Journal   (Followers: 22)
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)
Avicenna Journal of Medical Biochemistry     Open Access  
Bangladesh Journal of Medical Biochemistry     Open Access   (Followers: 2)
BBA Clinical     Open Access  
BBR : Biochemistry and Biotechnology Reports     Open Access   (Followers: 4)
Biocatalysis     Open Access  
Biochemical and Biophysical Research Communications     Hybrid Journal   (Followers: 19)
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: 26)
Biochemical Pharmacology     Hybrid Journal   (Followers: 8)
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: 241)
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     Full-text available via subscription   (Followers: 15)
Biochemistry and Molecular Biology Education     Hybrid Journal   (Followers: 5)
Biochemistry and Molecular Biology of Fishes     Full-text available via subscription   (Followers: 1)
Biochemistry Research International     Open Access   (Followers: 5)
Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids     Hybrid Journal   (Followers: 9)
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease     Hybrid Journal   (Followers: 16)
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research     Hybrid Journal   (Followers: 7)
Biochimie     Hybrid Journal   (Followers: 6)
Biochimie Open     Open Access  
Bioconjugate Chemistry     Full-text available via subscription   (Followers: 30)
BioDrugs     Full-text available via subscription   (Followers: 8)
Bioelectrochemistry     Hybrid Journal   (Followers: 2)
Biofuels     Hybrid Journal   (Followers: 10)
Biogeochemistry     Hybrid Journal   (Followers: 11)
BioInorganic Reaction Mechanisms     Hybrid Journal   (Followers: 1)
Biokemistri     Open Access  
Biological Chemistry     Partially Free   (Followers: 25)
Biomaterials Research     Open Access   (Followers: 4)
Biomedicines     Open Access   (Followers: 1)
BioMolecular Concepts     Hybrid Journal   (Followers: 2)
Bioscience, Biotechnology, and Biochemistry     Hybrid Journal   (Followers: 25)
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  
Carbohydrate Polymers     Hybrid Journal   (Followers: 7)
Cell Biochemistry and Biophysics     Hybrid Journal   (Followers: 5)
Cell Biochemistry and Function     Hybrid Journal   (Followers: 4)
Cellular Physiology and Biochemistry     Open Access   (Followers: 3)
ChemBioChem     Hybrid Journal   (Followers: 6)
Chemical and Biological Technologies for Agriculture     Open Access  
Chemical Biology & Drug Design     Hybrid Journal   (Followers: 22)
Chemical Engineering Journal     Hybrid Journal   (Followers: 30)
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: 5)
Chemistry & Biology     Full-text available via subscription   (Followers: 29)
Chemistry and Ecology     Hybrid Journal  
ChemTexts     Hybrid Journal  
Clinica Chimica Acta     Hybrid Journal   (Followers: 36)
Clinical Biochemist Reviews     Full-text available via subscription   (Followers: 1)
Clinical Biochemistry     Hybrid Journal   (Followers: 19)
Clinical Chemistry     Full-text available via subscription   (Followers: 67)
Clinical Chemistry and Laboratory Medicine     Hybrid Journal   (Followers: 61)
Clinical Lipidology     Full-text available via subscription  
Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology     Hybrid Journal   (Followers: 5)
Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology     Hybrid Journal   (Followers: 2)
Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology     Hybrid Journal   (Followers: 7)
Comparative Biochemistry and Physiology Part D: Genomics and Proteomics     Hybrid Journal   (Followers: 3)
Comprehensive Biochemistry     Full-text available via subscription   (Followers: 1)
Computational Biology and Chemistry     Hybrid Journal   (Followers: 10)
Critical Reviews in Biochemistry and Molecular Biology     Hybrid Journal   (Followers: 5)
Current Chemical Biology     Hybrid Journal   (Followers: 2)
Current Medicinal Chemistry     Hybrid Journal   (Followers: 15)
Current Opinion in Chemical Biology     Hybrid Journal   (Followers: 24)
Current Opinion in Lipidology     Hybrid Journal   (Followers: 5)
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: 59)
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: 3)
Frontiers in Molecular Biosciences     Open Access   (Followers: 2)
Frontiers in Natural Product Chemistry     Hybrid Journal  
Global Biogeochemical Cycles     Full-text available via subscription   (Followers: 12)
Green Chemistry     Full-text available via subscription   (Followers: 9)
Histochemistry and Cell Biology     Hybrid Journal   (Followers: 4)
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: 7)
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  
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: 5)
Journal of Microbial & Biochemical Technology     Open Access   (Followers: 1)
Journal of Applied Biology & Biotechnology     Open Access   (Followers: 1)
Journal of Bioactive and Compatible Polymers     Hybrid Journal   (Followers: 2)
Journal of Biochemistry     Hybrid Journal   (Followers: 44)
Journal of Biological Chemistry     Full-text available via subscription   (Followers: 179)
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: 1)
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   (Followers: 1)
Journal of Enzyme Inhibition and Medicinal Chemistry     Hybrid Journal   (Followers: 4)
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: 3)
Journal of Inborn Errors of Metabolism and Screening     Open Access  
Journal of Inorganic Biochemistry     Hybrid Journal   (Followers: 5)
Journal of Investigational Biochemistry     Open Access   (Followers: 2)
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: 3)
Journal of Nutritional Biochemistry     Hybrid Journal   (Followers: 7)
Journal of Pediatric Biochemistry     Hybrid Journal   (Followers: 1)
Journal of Peptide Science     Hybrid Journal   (Followers: 23)
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: 5)
Journal of Steroid Biochemistry and Molecular Biology     Hybrid Journal   (Followers: 2)
Journal of Virology & Antiviral Research     Hybrid Journal   (Followers: 3)
Journal of Wood Chemistry and Technology     Hybrid Journal   (Followers: 7)
La Rivista Italiana della Medicina di Laboratorio - Italian Journal of Laboratory Medicine     Hybrid Journal  
Lab on a Chip     Full-text available via subscription   (Followers: 34)
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: 4)
Molecular Aspects of Medicine     Hybrid Journal   (Followers: 5)
Molecular Informatics     Hybrid Journal   (Followers: 4)
Molecular inhibitors in targeted therapy     Open Access  
Moscow University Chemistry Bulletin     Hybrid Journal   (Followers: 1)
Mycology : An International Journal on Fungal Biology     Hybrid Journal   (Followers: 5)
Natural Products and Bioprospecting     Open Access   (Followers: 3)
Nature Chemical Biology     Full-text available via subscription   (Followers: 69)
Nature Communications     Open Access   (Followers: 123)
Neurosignals     Open Access  
Novelty in Biomedicine     Open Access  
Ocean Acidification     Open Access   (Followers: 3)
Organic & Biomolecular Chemistry     Full-text available via subscription   (Followers: 86)
Peptidomics     Open Access  
Pesticide Biochemistry and Physiology     Hybrid Journal   (Followers: 4)
Pflugers Archiv European Journal of Physiology     Hybrid Journal   (Followers: 3)
Pharmaceutical Bioprocessing     Full-text available via subscription   (Followers: 1)
Pharmacognosy Magazine     Open Access   (Followers: 2)

        1 2     

Journal Cover Archives of Biochemistry and Biophysics
  [SJR: 1.478]   [H-I: 138]   [22 followers]  Follow
    
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 0003-9861 - ISSN (Online) 1096-0384
   Published by Elsevier Homepage  [3039 journals]
  • Structural and functional studies of the Leishmania braziliensis
           mitochondrial Hsp70: Similarities and dissimilarities to human orthologues
           
    • Authors: Paulo R. Dores-Silva; Letícia S. Nishimura; Vanessa T.R. Kiraly; Júlio C. Borges
      Pages: 43 - 52
      Abstract: Publication date: 1 January 2017
      Source:Archives of Biochemistry and Biophysics, Volume 613
      Author(s): Paulo R. Dores-Silva, Letícia S. Nishimura, Vanessa T.R. Kiraly, Júlio C. Borges
      Heat shock protein 70 kDa (Hsp70) is a conserved molecular chaperone family involved in several functions related to protein homeostasis. In eukaryotes, Hsp70 homologues are found in all cell compartments. The mitochondrial Hsp70 isoform (mtHsp70) is involved in import of mitochondrial matrix proteins as well as their folding and maturation. Moreover, mtHsp70 has the propensity to self-aggregate, and it depends on the action of the co-chaperone Hsp70-escort protein 1 (Hep1) to be produced functional. Here, we analyze the solution structure and function of mtHsp70 of Leishmania braziliensis (LbmtHsp70). This recombinant protein was obtained folded, in the monomeric state and it has an elongated shape. We observed that LbmtHsp70 suffers thermal aggregation that depends on the protein concentration and is composed of domains with different thermal stabilities. LbmtHsp70 interacted with adenosine nucleotides with a thermodynamic signature different from those reported for human orthologues and interacted, driven by both enthalpy and entropy, with L. braziliensis Hep1 (LbHep1) with a nanomolar dissociation constant. Moreover, LbHep1 stimulated the LbmtHsp70 ATPase activity. Since little is known about mitochondrial Hsp70, particularly in protozoa, we believe that our data are of interest for understanding protozoan Hsp70 machinery.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.11.004
      Issue No: Vol. 613 (2016)
       
  • Crystal structures of the CO and NOBound DosS GAF-A domain and
           implications for DosS signaling in Mycobacterium tuberculosis
    • Authors: Yarrow Madrona; Christopher A. Waddling; Paul R. Ortiz de Montellano
      Pages: 1 - 8
      Abstract: Publication date: 15 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 612
      Author(s): Yarrow Madrona, Christopher A. Waddling, Paul R. Ortiz de Montellano
      DosS is a sensor in Mycobacterium tuberculosis that differentially responds to O2, NO, and CO, as well as to changes in the redox state of the prosthetic heme iron atom. The ferrous protein and its Fe(II)NO and Fe(II)CO complexes undergo autophosphorylation and subsequently transfer the phosphate group to DosR, a nuclear factor, to activate it. In contrast, autophosphorylation is negligible with the ferric protein and the Fe(II)O2 complex. To clarify the basis for this differential response to gases, we have determined the crystal structures of the NO and COcomplexes of the DosS GAF-A domain, which contains the heme to which the gases bind. Comparison of these crystal structures with those reported for the phosphorylation-inactive ferric GAF-A domain suggest that the GAF-A domain is in a dynamic equilibrium between active and inactive states, and that the position of Glu87 in the heme cavity, which depends on the which gas is bound, acts as a modulator of the equilibrium, and therefore of catalytic activity.
      Graphical abstract image

      PubDate: 2016-10-13T16:34:04Z
      DOI: 10.1016/j.abb.2016.10.005
      Issue No: Vol. 612 (2016)
       
  • Insight into the impact of two structural calcium ions on the properties
           of Pleurotus eryngii versatile ligninolytic peroxidase
    • Authors: Yu Gao; Lanyan Zheng; Jian-Jun Li; Yuguang Du
      Pages: 9 - 16
      Abstract: Publication date: Available online 5 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Yu Gao, Lanyan Zheng, Jian-Jun Li, Yuguang du
      Two structural Ca2+ (proximal and distal) is known to be important for ligninolytic peroxidases. However, few studies toward impact of residues involved in two Ca2+ on properties of ligninolytic peroxidases have been done, especially the proximal one. In this study, mutants of nine residues involved in liganding two Ca2+ of Pleurotus eryngii versatile peroxidase (VP) were investigated. Most mutants almost completely lost activities, except the mutants of proximal Ca2+ - S170A and V192T. In comparison with WT (wild type), optimal pH values of S170A, S170D, and V192T shifted from pH 3.0 to pH 3.5. The order of thermal and pH stabilities of WT, V192T, S170A, and S170D is similar to that of their specific activities: WT > V192T > S170A > S170D. The CD (circular dichroism) results of WT and several mutants indicated that mutations had some effects on secondary structures. For the first time, it was observed that the thermostability of ligninolytic peroxidases is related with proximal Ca2+ too, and the mutant containing distal Ca2+ only was obtained. Our results clearly demonstrated that enzymatic activities, pH and thermal stabilities, Ca2+content, and secondary structures of VP have close relationship with the residues involved in two structural Ca2+.

      PubDate: 2016-10-06T16:07:59Z
      DOI: 10.1016/j.abb.2016.10.004
      Issue No: Vol. 612 (2016)
       
  • Insights into kinetic mechanism of Janus kinase 3 and its inhibition by
           tofacitinib
    • Authors: Mohammad Hekmatnejad; Sara Conwell; Stephen M. Lok; Alan Kutach; David Shaw; Eric Fang; David C. Swinney
      Pages: 22 - 34
      Abstract: Publication date: 15 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 612
      Author(s): Mohammad Hekmatnejad, Sara Conwell, Stephen M. Lok, Alan Kutach, David Shaw, Eric Fang, David C. Swinney
      JAK3 kinase plays a critical role in several cytokine signaling pathways involved in immune cell development and function. The studies presented in this report were undertaken to elucidate the kinetic mechanism of the JAK3 kinase domain, investigate the role of activation loop phosphorylation in regulating its catalytic activity, and examine its inhibition by the anti-rheumatoid arthritis drug, tofacitinib. Phosphorylation of two Tyr residues in JAK3's activation loop has been reported to impact its kinase activity. The recombinant JAK3 kinase domain used in our studies was heterogeneous in its activation loop phosphorylation, with the non-phosphorylated protein being the dominant species. Kinetic analysis revealed similar kinetic parameters for the heterogeneously phosphorylated JAK3, JAK3 mono-phosphorylated on Tyr 980, and the activation loop mutant YY980/981FF. Bisubstrate and product inhibition kinetic results were consistent with both sequential random and sequential ordered kinetic mechanisms. Solvent viscosometric experiments showed perturbation of k cat, suggesting the phosphoryl transfer step is not likely rate limiting. This was supported by results from quench-flow experiments, where a rapid burst of product formation was observed. Kinetic analysis of JAK3 inhibition by tofacitinib indicated inhibition is time dependent, characterized by on- and off-rate constants of 1.4 ± 0.1 μM−1s−1 and 0.0016 ± 0.0005 s−1, respectively.

      PubDate: 2016-10-19T12:26:14Z
      DOI: 10.1016/j.abb.2016.08.012
      Issue No: Vol. 612 (2016)
       
  • Steady-state kinetic studies reveal that the anti-cancer target
           Ubiquitin-Specific Protease 17 (USP17) is a highly efficient
           deubiquitinating enzyme
    • Authors: Nicole M. Hjortland; Andrew D. Mesecar
      Pages: 35 - 45
      Abstract: Publication date: Available online 15 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Nicole M. Hjortland, Andrew D. Mesecar
      USP17 is a deubiquitinating enzyme that is upregulated in numerous cancers and therefore a drug target. We developed a robust expression, purification, and assay system for USP17 enabling its enzymatic and structural characterization. USP17 was expressed in E. coli as inclusion bodies and then solubilized, refolded, and purified using affinity and size-exclusion chromatography. Milligram quantities of pure USP17 can be produced that is catalytically more efficient (kcat/Km = 1500 (x103) M−1 sec−1) than other human USPs studied to date. Analytical size-exclusion chromatography, analytical ultracentrifugation, and dynamic light scattering studies suggest that the quaternary structure of USP17 is a monomer. Steady-state kinetic studies show that USP17 efficiently hydrolyzes both ubiquitin-AMC (kcat = 1.5 sec−1 and Km = 1.0 μM) and ubiquitin-rhodamine110 (kcat = 1.8 sec−1 and Km = 2.0 μM) substrates. Ubiquitin chain cleavage assays reveal that USP17 efficiently cleaves di-ubiquitin chains with Lys11, Lys33, Lys48 and Lys63 linkages and tetra-ubiquitin chains with Lys11, Lys48 and Lys63 linkages but is inefficient in cleaving di-ubiquitin chains with Lys6, Lys27, or Lys29 linkages or linear ubiquitin chains. The substrate specificity of USP17 is most similar to that of USP1, where both USPs display higher specificity than other characterized members of the USP family.
      Graphical abstract image

      PubDate: 2016-10-19T12:26:14Z
      DOI: 10.1016/j.abb.2016.10.008
      Issue No: Vol. 612 (2016)
       
  • Corrigendum to “CD147 induces up-regulation of vascular endothelial
           growth factor in U937-derived foam cells through PI3K/AKT pathway”
           [Arch. Biochem. Biophys. 609 (2016) 31–38]
    • Authors: JiaXin Zong; YunTian Li; DaYong Du; Yang Liu; YongJun Yin
      First page: 120
      Abstract: Publication date: 15 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 612
      Author(s): JiaXin Zong, YunTian Li, DaYong Du, Yang Liu, YongJun Yin


      PubDate: 2016-11-23T15:43:39Z
      DOI: 10.1016/j.abb.2016.10.006
      Issue No: Vol. 612 (2016)
       
  • Editorial: The cutting edge of zinc biology
    • Authors: Taiho Kambe; Toshiyuki Fukada; Shinya Toyokuni
      Pages: 1 - 2
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Taiho Kambe, Toshiyuki Fukada, Shinya Toyokuni


      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.09.006
      Issue No: Vol. 611 (2016)
       
  • The biological inorganic chemistry of zinc ions
    • Authors: Artur Krężel; Wolfgang Maret
      Pages: 3 - 19
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Artur Krężel, Wolfgang Maret
      The solution and complexation chemistry of zinc ions is the basis for zinc biology. In living organisms, zinc is redox-inert and has only one valence state: Zn(II). Its coordination environment in proteins is limited by oxygen, nitrogen, and sulfur donors from the side chains of a few amino acids. In an estimated 10% of all human proteins, zinc has a catalytic or structural function and remains bound during the lifetime of the protein. However, in other proteins zinc ions bind reversibly with dissociation and association rates commensurate with the requirements in regulation, transport, transfer, sensing, signalling, and storage. In contrast to the extensive knowledge about zinc proteins, the coordination chemistry of the “mobile” zinc ions in these processes, i.e. when not bound to proteins, is virtually unexplored and the mechanisms of ligand exchange are poorly understood. Knowledge of the biological inorganic chemistry of zinc ions is essential for understanding its cellular biology and for designing complexes that deliver zinc to proteins and chelating agents that remove zinc from proteins, for detecting zinc ion species by qualitative and quantitative analysis, and for proper planning and execution of experiments involving zinc ions and nanoparticles such as zinc oxide (ZnO). In most investigations, reference is made to zinc or Zn2+ without full appreciation of how biological zinc ions are buffered and how the d-block cation Zn2+ differs from s-block cations such as Ca2+ with regard to significantly higher affinity for ligands, preference for the donor atoms of ligands, and coordination dynamics. Zinc needs to be tightly controlled. The interaction with low molecular weight ligands such as water and inorganic and organic anions is highly relevant to its biology but in contrast to its coordination in proteins has not been discussed in the biochemical literature. From the discussion in this article, it is becoming evident that zinc ion speciation is important in zinc biochemistry and for biological recognition as a variety of low molecular weight zinc complexes have already been implicated in biological processes, e.g. with ATP, glutathione, citrate, ethylenediaminedisuccinic acid, nicotianamine, or bacillithiol.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.04.010
      Issue No: Vol. 611 (2016)
       
  • Techniques for measuring cellular zinc
    • Authors: Margaret C. Carpenter; Maria N. Lo; Amy E. Palmer
      Pages: 20 - 29
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Margaret C. Carpenter, Maria N. Lo, Amy E. Palmer
      The development and improvement of fluorescent Zn2+ sensors and Zn2+ imaging techniques have increased our insight into this biologically important ion. Application of these tools has identified an intracellular labile Zn2+ pool and cultivated further interest in defining the distribution and dynamics of labile Zn2+. The study of Zn2+ in live cells in real time using sensors is a powerful way to answer complex biological questions. In this review, we highlight newly engineered Zn2+ sensors, methods to test whether the sensors are accessing labile Zn2+, and recent studies that point to the challenges of using such sensors. Elemental mapping techniques can complement and strengthen data collected with sensors. Both mass spectrometry-based and X-ray fluorescence-based techniques yield highly specific, sensitive, and spatially resolved snapshots of metal distribution in cells. The study of Zn2+ has already led to new insight into all phases of life from fertilization of the egg to life-threatening cancers. In order to continue building new knowledge about Zn2+ biology it remains important to critically assess the available toolset for this endeavor.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.08.018
      Issue No: Vol. 611 (2016)
       
  • Zinc sensing and regulation in yeast model systems
    • Authors: Stevin Wilson; Amanda J. Bird
      Pages: 30 - 36
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Stevin Wilson, Amanda J. Bird
      The Zap1 transcription factor of Saccharomyces cerevisiae and the Loz1 transcription factor of Schizosaccharomyces pombe both play a central role in zinc homeostasis by controlling the expression of genes necessary for zinc metabolism. Zap1 activates gene expression when cells are limited for zinc, while Loz1 is required for gene repression when zinc is in excess. In this review we highlight what is known about the underlying mechanisms by which these factors are regulated by zinc, and how transcriptional activation and repression in eukaryotic cells can be finely tuned according to intracellular zinc availability.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.02.031
      Issue No: Vol. 611 (2016)
       
  • Activation of zinc-requiring ectoenzymes by ZnT transporters during the
           secretory process: Biochemical and molecular aspects
    • Authors: Taiho Kambe; Taka-aki Takeda; Yukina Nishito
      Pages: 37 - 42
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Taiho Kambe, Taka-aki Takeda, Yukina Nishito
      In humans, about 1000 enzymes are estimated to bind zinc. In most of these enzymes, zinc is present at the active site; thus, these enzymes are functional as “zinc-requiring enzymes”. Of these zinc-requiring enzymes, zinc-requiring ectoenzymes (defined as secretory, membrane-bound, and organelle-resident enzymes) have received much attention because of their important physiological functions, involvement in a number of diseases, and potential applications as therapeutic targets for diseases. Zinc-requiring ectoenzymes may become active by coordinating zinc at their active site during the secretory process, which requires elaborate control of zinc mobilization from the extracellular milieu to the cytosol and then lumen in the early secretory pathway. Therefore, zinc transporters should properly maintain the process at systemic, cellular, and subcellular levels by mobilizing zinc across biological membranes. However, few studies have examined the mechanisms underlying this process. In this review, current knowledge of the activation process of zinc-requiring ectoenzymes by ZnT zinc transporters in the early secretory pathway is briefly reviewed at the molecular level, with a focus on tissue-nonspecific alkaline phosphatase. Moreover, we also discuss whether zinc-chaperone proteins function during the activation of these enzymes.
      Graphical abstract image

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.03.035
      Issue No: Vol. 611 (2016)
       
  • Zinc transporters and signaling in physiology and pathogenesis
    • Authors: Shintaro Hojyo; Toshiyuki Fukada
      Pages: 43 - 50
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Shintaro Hojyo, Toshiyuki Fukada
      Zinc (Zn) is an essential trace element that is vital in a wide range of cellular machineries because of its effect on the expression and activity of various transcription factors and enzymes. Zn deficiency disturbs Zn homeostasis and has pathogenic consequences, including growth retardation and immune impairment in mammals. Zn homeostasis is tightly controlled by the coordinated activity of Zn transporters and metallothioneins, which regulate the distribution, storage, and intracellular and extracellular concentration of Zn. Recent reverse-genetic approaches using Zn transporter–deficient mice have revealed the physiological functions of specific Zn signaling axes (each formed by Zn and a Zn transporter) in various biological programs. In this review, we describe recent discoveries about the role of Zn transporters which facilitate cellular signaling through Zn uptake in physiology and pathogenesis, with particular focus on the influence of Zn signaling in systemic growth and immunity.
      Graphical abstract image

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.06.020
      Issue No: Vol. 611 (2016)
       
  • Zinc and infant nutrition
    • Authors: M. Leigh Ackland; Agnes A. Michalczyk
      Pages: 51 - 57
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): M. Leigh Ackland, Agnes A. Michalczyk
      Zinc is essential for a wide variety of cellular processes in all cells. It is a critical dietary nutrient, particularly in the early stages of life. In the early neonatal period, adequate sources of zinc can be obtained from breast milk. In rare circumstances, the mammary gland produces zinc deficient milk that is potentially lethal for exclusively breast-fed infants. This can be overcome by zinc supplementation to the infant. Alterations to key zinc transporters provide insights into the mechanisms of cellular zinc homeostasis. The bioavailability of zinc in food depends on the presence of constituents that may complex zinc. In many countries, zinc deficiency is a major health issue due to poor nourishment. Young children are particularly affected. Zinc deficiency can impair immune function and contributes to the global burden of infectious diseases including diarrhoea, pneumonia and malaria. Furthermore, zinc deficiency may extend its influence across generations by inducing epigenetic effects that alter the expression of genes. This review discusses the significance of adequate zinc nutrition in infants, factors that influence zinc nutrition, the consequences of zinc deficiency, including its contribution to the global burden of disease, and addresses some of the knowledge gaps in zinc biology.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.06.011
      Issue No: Vol. 611 (2016)
       
  • Zinc and immunity: An essential interrelation
    • Authors: Maria Maares; Hajo Haase
      Pages: 58 - 65
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Maria Maares, Hajo Haase
      The significance of the essential trace element zinc for immune function has been known for several decades. Zinc deficiency affects immune cells, resulting in altered host defense, increased risk of inflammation, and even death. The micronutrient zinc is important for maintenance and development of immune cells of both the innate and adaptive immune system. A disrupted zinc homeostasis affects these cells, leading to impaired formation, activation, and maturation of lymphocytes, disturbed intercellular communication via cytokines, and weakened innate host defense via phagocytosis and oxidative burst. This review outlines the connection between zinc and immunity by giving a survey on the major roles of zinc in immune cell function, and their potential consequences in vivo.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.03.022
      Issue No: Vol. 611 (2016)
       
  • Immunological orchestration of zinc homeostasis: The battle between host
           mechanisms and pathogen defenses
    • Authors: Kavitha Subramanian Vignesh; George S. Deepe
      Pages: 66 - 78
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Kavitha Subramanian Vignesh, George S. Deepe
      The importance of Zn ions (Zn) in regulating development and functions of the immune system is well established. However, recent years have witnessed a surge in our knowledge of how immune cells choreograph Zn regulatory mechanisms to combat the persistence of pathogenic microbes. Myeloid and lymphoid populations manipulate intracellular and extracellular Zn metabolism via Zn binding proteins and transporters in response to immunological signals and infection. Rapid as well as delayed changes in readily exchangeable Zn, also known as free Zn and the Zn proteome are crucial in determining activation of immune cells, cytokine responses, signaling and nutritional immunity. Recent studies have unearthed distinctive Zn modulatory mechanisms employed by specialized immune cells and necessitate an understanding of the Zn handling behavior in immune responses to infection. The focus of this review, therefore, stems from novel revelations of Zn intoxication, sequestration and signaling roles deployed by different immune cells, with an emphasis on innate immunity, to challenge microbial parasitization and cope with pathogen insult.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.02.020
      Issue No: Vol. 611 (2016)
       
  • Zinc and diabetes
    • Authors: Pauline Chabosseau; Guy A. Rutter
      Pages: 79 - 85
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Pauline Chabosseau, Guy A. Rutter
      Zn2+ ions are essential for the normal processing and storage of insulin and altered pancreatic insulin content is associated with all forms of diabetes mellitus. Work of the past decade has identified variants in the human SLC30A8 gene, encoding the zinc transporter ZnT8 which is expressed highly selectively on the secretory granule of pancreatic islet β and α cells, as affecting the risk of Type 2 Diabetes. Here, we review the regulation and roles of Zn2+ ions in islet cells, the mechanisms through which SLC30A8 variants might affect glucose homeostasis and diabetes risk, and the novel technologies including recombinant targeted zinc probes and knockout mice which have been developed to explore these questions.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.05.022
      Issue No: Vol. 611 (2016)
       
  • Molecular regulation of lactation: The complex and requisite roles for
           zinc
    • Authors: Sooyeon Lee; Shannon L. Kelleher
      Pages: 86 - 92
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Sooyeon Lee, Shannon L. Kelleher
      Lactation provides many health benefits to the nursing infant and breastfeeding mother. In order to successfully breastfeed, the mammary gland must expand and differentiate to activate numerous processes that regulate milk production and secretion. This involves a complex series of molecular, biochemical and cellular events driven largely by lactogenic hormones. Recent advances implicate zinc as a critical modulator of mammary gland function. Here, we provide an overview of our current understanding of the role and regulation of zinc in promoting proliferation, differentiation and secretion in the mammary gland during lactation, and highlight critical gaps in knowledge.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.04.002
      Issue No: Vol. 611 (2016)
       
  • Insight into cognitive decline from Zn2+ dynamics through extracellular
           signaling of glutamate and glucocorticoids
    • Authors: Atsushi Takeda; Hanuna Tamano
      Pages: 93 - 99
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Atsushi Takeda, Hanuna Tamano
      Glutamatergic neuron activity and/or the modification of the activity with glucocorticoids are closely linked to synaptic Zn2+ dynamics as well as synaptic Ca2+ dynamics. The dynamic crosstalk of synaptic Zn2+ signaling to intracellular Ca2+ signaling via calcium channels is involved in synaptic plasticity such as long-term potentiation (LTP) and cognitive activity. The influx of extracellular Zn2+ into postsynaptic neurons, which is closely linked to glutamate signaling in the synaptic cleft, is critical for cognitive activity. However, excess intracellular Zn2+ signaling induced by excess glutamatergic neuron activity is involved in not only cognitive decline in neurological disorders but also stress-induced cognitive decline. On the other hand, it has been recognized that excess Ca2+ influx into postsynaptic neurons induces neuronal death, while the involvement of excess intracellular Ca2+ signaling in cognitive decline is poorly understood. Understanding of synaptic Zn2+ dynamics, which are modified by glutamate and glucocorticoid signaling, may be meaningful to prevent Zn2+-mediated cognitive decline. This paper summarizes the current knowledge on Zn2+ dynamics under changing synaptic environment and its impact on cognitive decline.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.06.021
      Issue No: Vol. 611 (2016)
       
  • A comprehensive review of the role of zinc in normal prostate function and
           metabolism; and its implications in prostate cancer
    • Authors: Leslie C. Costello; Renty B. Franklin
      Pages: 100 - 112
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Leslie C. Costello, Renty B. Franklin
      The human prostate gland contains extremely high zinc levels; which is due to the specialized zinc-accumulating acinar epithelial of the peripheral zone. These cells evolved for their unique capability to produce and secrete extremely levels of citrate, which is achieved by the high cellular zinc level effects on the cell metabolism. This review highlights the specific functional and metabolic alterations that result from the accumulation of the high zinc levels, especially its effects on mitochondrial citrate metabolism and terminal oxidation. The implications of zinc in the development and progression of prostate cancer are described, which is the most consistent hallmark characteristic of prostate cancer. The requirement for decreased zinc resulting from down regulation of ZIP1 to prevent zinc cytotoxicity in the malignant cells is described as an essential early event in prostate oncogenesis. This provides the basis for the concept that an agent (such as the zinc ionophore, clioquinol) that facilitates zinc uptake and accumulation in ZIP1-deficient prostate tumors cells will markedly inhibit tumor growth. In the current absence of an efficacious chemotherapy for advanced prostate cancer, and for prevention of early development of malignancy; a zinc treatment regimen is a plausible approach that should be pursued.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.04.014
      Issue No: Vol. 611 (2016)
       
  • Zinc and skin biology
    • Authors: Youichi Ogawa; Tatsuyoshi Kawamura; Shinji Shimada
      Pages: 113 - 119
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Youichi Ogawa, Tatsuyoshi Kawamura, Shinji Shimada
      Of all tissues, the skin has the third highest abundance of zinc in the body. In the skin, the zinc concentration is higher in the epidermis than in the dermis, owing to a zinc requirement for the active proliferation and differentiation of epidermal keratinocytes. Here we review the dynamics and functions of zinc in the skin as well as skin disorders associated with zinc deficiency, zinc finger domain-containing proteins, and zinc transporters. Among skin disorders associated with zinc deficiency, acrodermatitis enteropathica is a disorder caused by mutations in the ZIP4 transporter and subsequent zinc deficiency. The triad acrodermatitis enteropathica is characterized by alopecia, diarrhea, and skin lesions in acral, periorificial, and anogenital areas. We highlight the underlying mechanism of the development of acrodermatitis because of zinc deficiency by describing our new findings. We also discuss the accumulating evidence on zinc deficiency in alopecia and necrolytic migratory erythema, which is typically associated with glucagonomas.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.06.003
      Issue No: Vol. 611 (2016)
       
  • Insights into zinc and cadmium biology in the nematode Caenorhabditis
           elegans
    • Authors: Nicholas Dietrich; Chieh-Hsiang Tan; Ciro Cubillas; Brian James Earley; Kerry Kornfeld
      Pages: 120 - 133
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Nicholas Dietrich, Chieh-Hsiang Tan, Ciro Cubillas, Brian James Earley, Kerry Kornfeld
      Zinc is an essential metal that is involved in a wide range of biological processes, and aberrant zinc homeostasis is implicated in multiple human diseases. Cadmium is chemically similar to zinc, but it is a nonessential environmental pollutant. Because zinc deficiency and excess are deleterious, animals require homeostatic mechanisms to maintain zinc levels in response to dietary fluctuations. The nematode Caenorhabditis elegans is emerging as a powerful model system to investigate zinc trafficking and homeostasis as well as cadmium toxicity. Here we review genetic and molecular studies that have combined to generate a picture of zinc homeostasis based on the transcriptional control of zinc transporters in intestinal cells. Furthermore, we summarize studies of cadmium toxicity that reveal intriguing parallels with zinc biology.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.05.021
      Issue No: Vol. 611 (2016)
       
  • What can flies tell us about zinc homeostasis'
    • Authors: Guiran Xiao; Bing Zhou
      Pages: 134 - 141
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Guiran Xiao, Bing Zhou
      Zinc is an essential micronutrient for all organisms. For multicellular organisms, zinc uptake, storage, distribution and export are tightly regulated at both cellular and organismal levels, to cope with the multiple requirements versus the toxicity of the metal ion. During the past decade, the fruit fly Drosophila melanogaster has become an important model organism for the elucidation of metazoan zinc homeostasis. This review describes our current knowledge of various zinc transporters in Drosophila, with an emphasis on the process of dietary zinc uptake in the fly. We also discuss how Drosophila was used as a model to facilitate our understanding of the role of zinc in neurodegenerative diseases.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.04.016
      Issue No: Vol. 611 (2016)
       
  • A fly's eye view of zinc homeostasis: Novel insights into the genetic
           control of zinc metabolism from Drosophila
    • Authors: Christopher D. Richards; Richard Burke
      Pages: 142 - 149
      Abstract: Publication date: 1 December 2016
      Source:Archives of Biochemistry and Biophysics, Volume 611
      Author(s): Christopher D. Richards, Richard Burke
      The core zinc transport machinery is well conserved between invertebrates and mammals, with the vinegar fly Drosophila melanogaster having clear homologues of all major groups of mammalian ZIP and ZNT transport genes. Functional characterization of several of the fly genes has revealed functional conservation between related fly and mammalian zinc transporters in some but not all cases, indicating that Drosophila is a useful model for examining mammalian zinc metabolism. Furthermore, Drosophila research, sometimes quite serendipitously, has provided novel insights into the function of zinc transporters and into zinc-related pathologies, which are highlighted here. Finally, the future research potential of the fly in nutrient metabolism is explored, with reference to emerging experimental technologies.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.07.015
      Issue No: Vol. 611 (2016)
       
  • The lncRNA H19 interacts with miR-140 to modulate glioma growth by
           targeting iASPP
    • Authors: Haiting Zhao; Renjun Peng; Qing Liu; Dingyang Liu; Peng Du; Jian Yuan; Gang Peng; Yiwei Liao
      Pages: 1 - 7
      Abstract: Publication date: Available online 28 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Haiting Zhao, Renjun Peng, Qing Liu, Dingyang Liu, Peng Du, Jian Yuan, Gang Peng, Yiwei Liao
      H19, one of the first found cancer-associated long non-coding RNAs (lncRNAs), is involved in the development and progression of many types of tumors. An aberrant expression of H19 was observed in hepatocellular carcinoma, cervical cancer, breast cancer, ovarian cancer, and colorectal cancer. However, the exact effects and molecular mechanisms of H19 in glioma progression are still unknown up to now. In this study, we investigated the role of H19 in human glioma cell lines and clinical tumor samples in order to determine the function of this molecule. In our research, lncRNA-H19 was specifically upregulated in glioma cell lines and promoted glioma cell growth through targeting miR-140. Knockdown of H19 inhibited the proliferation and invasion of human glioma cell and suppressed its metastasis in vitro and in vivo. In addition, miR-140 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) regulation was required in H19 induced glioma cell growth. These findings indicated that H19 might regulate the tumor growth and metastasis via miR-140 dependent iASPP regulation. Taken together, our data indicated that H19 might be an oncogenic lncRNA that promoted proliferation and metastasis of glioma and could be regarded as a therapeutic target in human glioma.

      PubDate: 2016-09-30T16:01:00Z
      DOI: 10.1016/j.abb.2016.09.014
      Issue No: Vol. 610 (2016)
       
  • Olfactory signaling components and olfactory receptors are expressed in
           tubule cells of the human kidney
    • Authors: Benjamin Kalbe; Marian Schlimm; Sebastian Wojcik; Stathis Philippou; Désirée Maßberg; Fabian Jansen; Paul Scholz; Hermann Luebbert; Burkhard Ubrig; Sabrina Osterloh; Hanns Hatt
      Pages: 8 - 15
      Abstract: Publication date: Available online 28 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Benjamin Kalbe, Marian Schlimm, Sebastian Wojcik, Stathis Philippou, Désirée Maßberg, Fabian Jansen, Paul Scholz, Hermann Luebbert, Burkhard Ubrig, Sabrina Osterloh, Hanns Hatt
      Cells of the renal tubule system are in direct contact with compounds dissolved in the urine, such as short chain fatty acids (SCFA). Murine OR78, a member of the olfactory receptor (OR) family, is involved in SCFA-related regulation of renal blood pressure in mice. It is still unclear whether OR signaling has an impact on human renal physiology. In our study, we showed that OR51E1 and OR11H7, both of which can be activated by the SCFA isovaleric acid, are expressed in the HK-2 human proximal tubule cell line. We observed a transient increase in intracellular Ca2+ when isovaleric acid and 4-methylvaleric acid were added to HK-2 cells. The isovaleric acid-induced response was dependent on extracellular Ca2+ and adenylyl cyclase (AC) activation. Furthermore, we demonstrated that the canonical olfactory signaling components Gαolf and ACIII are co-localized with OR51E1. The number of cells responding to isovaleric acid correlated with the presence of primary cilia on HK-2 cells. OR51E1 protein expression was confirmed in the tubule system of human kidney tissue. Our study is the first to show the expression of ORs and olfactory signaling components in human kidney cells. Additionally, we discuss ORs as potential modulators of the renal physiology.

      PubDate: 2016-09-30T16:01:00Z
      DOI: 10.1016/j.abb.2016.09.017
      Issue No: Vol. 610 (2016)
       
  • High-fat diet feeding promotes stemness and precancerous changes in murine
           gastric mucosa mediated by leptin receptor signaling pathway
    • Authors: Seiya Arita; Yuta Kinoshita; Kaori Ushida; Atsushi Enomoto; Kyoko Inagaki-Ohara
      Pages: 16 - 24
      Abstract: Publication date: Available online 28 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Seiya Arita, Yuta Kinoshita, Kaori Ushida, Atsushi Enomoto, Kyoko Inagaki-Ohara
      Obesity increases the risk for gastric cancers. However, the occurrence and mechanisms of precancerous atrophic gastritis induced by high-fat diet (HFD) remain unclear. Here, we show that HFD-associated lipotoxicity induces precancerous lesions that are accompanied by the disruption of organelle homeostasis, tissue integrity, and deregulated expression of stemness genes in the gastric epithelium mediated by leptin receptor (ObR) signaling. Following HFD feeding, ectopic fat accumulated and expression of LAMP2A in lysosome and COX IV in mitochondria increased in the gastric mucosa. HFD feeding also led to enhanced expression of activated-Notch1 and stem cell markers Lgr5, CD44, and EpCAM. In addition, HFD-fed mice showed intracellular β-catenin accumulation in the gastric mucosa with increased expression of its target genes, Nanog, Oct4, and c-Myc. These observations were abrogated in the leptin-deficient ob/ob mice and ObR-mutated db/db mice, indicating that these HFD-induced changes were responsible for effects downstream of the ObR. Consistent with this, the expression of the Class IA and III PI3Ks was increased following ObR activation in the gastric mucosa of HFD-fed mice. Together, these results suggest that HFD-induced lipotoxicity and deregulated organelle biosynthesis confer cancer stem cell-like properties to the gastric mucosa via signaling pathway mediated by leptin, PI3K and β-catenin.

      PubDate: 2016-09-30T16:01:00Z
      DOI: 10.1016/j.abb.2016.09.015
      Issue No: Vol. 610 (2016)
       
  • Real-time monitoring of artemin in vivo chaperone activity using
           luciferase as an intracellular reporter
    • Authors: Zeinab Takalloo; Reza H. Sajedi; Saman Hosseinkhani; S. Mohsen Asghari
      Pages: 33 - 40
      Abstract: Publication date: Available online 28 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Zeinab Takalloo, Reza H. Sajedi, Saman Hosseinkhani, S. Mohsen Asghari
      Artemin is an abundant thermostable protein in Artemia encysted embryos and considered as a stress protein, as its highly regulated expression is associated with stress resistance. Artemin cDNA was previously isolated and cloned from Artemia urmiana and artemin was found as an efficient molecular chaperone in vitro. Here, co-transformation of E. coli was performed with two expression vectors containing artemin and firefly luciferase for in vivo studies. The time-course of luciferase inactivation at low and elevated temperatures showed that luciferase was rapidly inactivated in control cells, but it was found that luciferase was protected significantly in artemin expressing cells. More interestingly, luciferase activity was completely regained in heat treated artemin expressing cells at room temperature. In addition, in both stress conditions, similar to residual activity of luciferase, cell viability in induced cultures over-expressing artemin was significantly higher than non-expressed artemin cells. It can be suggested that artemin confers impressive resistance in stressful conditions when introduced into E. coli cells, which is due to that it protects proteins against aggregation. Such luciferase co-expression system can be used as a real-time reporter to investigate the activity of chaperone proteins in vivo and provide a rapid and simple test for molecular chaperones.
      Graphical abstract image

      PubDate: 2016-09-30T16:01:00Z
      DOI: 10.1016/j.abb.2016.09.016
      Issue No: Vol. 610 (2016)
       
  • The preferential heterodimerization of human small heat shock proteins
           HSPB1 and HSPB6 is dictated by the N-terminal domain
    • Authors: Michelle Heirbaut; Frederik Lermyte; Esther M. Martin; Steven Beelen; Tim Verschueren; Frank Sobott; Sergei V. Strelkov; Stephen D. Weeks
      Pages: 41 - 50
      Abstract: Publication date: Available online 4 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Michelle Heirbaut, Frederik Lermyte, Esther M. Martin, Steven Beelen, Tim Verschueren, Frank Sobott, Sergei V. Strelkov, Stephen D. Weeks
      Small heat shock proteins are ATP-independent molecular chaperones. Their function is to bind partially unfolded proteins under stress conditions. In vivo, members of this chaperone family are known to preferentially assemble together forming large, polydisperse heterooligomers. The exact molecular mechanisms that drive specific heteroassociation are currently unknown. Here we study the oligomers formed between human HSPB1 and HSPB6. Using small-angle X-ray scattering we could characterize two distinct heterooligomeric species present in solution. By employing native mass spectrometry we show that such assemblies are formed purely from heterodimeric building blocks, in line with earlier cross-linking studies. Crucially, a detailed analysis of truncation variants reveals that the preferential association between these two sHSPs is solely mediated by their disordered N-terminal domains.

      PubDate: 2016-10-06T16:07:59Z
      DOI: 10.1016/j.abb.2016.10.002
      Issue No: Vol. 610 (2016)
       
  • Appraisal of role of the polyanionic inducer length on amyloid formation
           by 412-residue 1N4R Tau protein: A comparative study
    • Authors: Abolfazl Jangholi; Mohammad Reza Ashrafi-Kooshk; Seyed Shahriar Arab; Gholamhossein Riazi; Farzad Mokhtari; Mansour Poorebrahim; Hamid Mahdiuni; Boris I. Kurganov; Ali Akbar Moosavi-Movahedi; Reza Khodarahmi
      Pages: 1 - 19
      Abstract: Publication date: Available online 13 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Abolfazl Jangholi, Mohammad Reza Ashrafi-Kooshk, Seyed Shahriar Arab, Gholamhossein Riazi, Farzad Mokhtari, Mansour Poorebrahim, Hamid Mahdiuni, Boris I. Kurganov, Ali Akbar Moosavi-Movahedi, Reza Khodarahmi
      In many neurodegenerative diseases, formation of protein fibrillar aggregates has been observed as a major pathological change. Neurofibrillary tangles, mainly composed of fibrils formed by the microtubule-associated protein; Tau, are a hallmark of a group of neurodegenerative diseases such as Alzheimer's disease. Tau belongs to the class of natively unfolded proteins and partially folds into an ordered β-structure during aggregation. Polyanionic cofactors such as heparin are commonly used as inducer of Tau aggregation in vitro. The role of heparin in nucleation and elongation steps during Tau fibril formation is not fully understood. In the current study, aggregation kinetics as well as structure of Tau amyloid fibrils, by using the 1N4R isoform, have been reproducibly determined in the presence of heparin and the shorter molecule; enoxaparin. The kinetic studies demonstrated that heparin (not enoxaparin) efficiently accelerates Tau amyloid formation and revealed, mechanistically, that the molecular weight of the inducer is important in accelerating amyloidogenesis. The kinetic parameter values of Tau amyloid aggregation, especially, the amyloid aggregation extent, were relatively different in the presence of heparin and enoxaparin, at various stoichiometries of the inducers binding. Also, based on the results, obtained from CD, FTIR, AFM and XRD studies, it may be suggested that the inducer length plays a critical role mainly in the nucleation process, so that it determines that oligomers lie on or off the pathway of Tau fibrillization. The biochemical results herein suggest that the chemical environment of the extracellular matrix as well as localization of distinct glycosaminoglycans may influence deposition behavior of Tau amyloidosis.
      Graphical abstract image

      PubDate: 2016-09-15T14:57:26Z
      DOI: 10.1016/j.abb.2016.09.004
      Issue No: Vol. 609 (2016)
       
  • Glycome complexity of human seminal plasma high molecular mass components:
           Evaluation of the contribution of acid-soluble glycoproteins/mucins and
           extracellular vesicles
    • Authors: Bojana Milutinovic; Ninoslav Mitic; Jelena Roncevic; Sanja Goc; Miroslava Jankovic
      Pages: 20 - 30
      Abstract: Publication date: 1 November 2016
      Source:Archives of Biochemistry and Biophysics, Volume 609
      Author(s): Bojana Milutinovic, Ninoslav Mitic, Jelena Roncevic, Sanja Goc, Miroslava Jankovic
      This study was aimed at evaluation of the contribution of acid-soluble glycoproteins (ASG)/mucins and extracellular vesicles (EVs), yet unexplored components of human seminal plasma (hSP) to the complexity of its glycome. Gaining insight into the native presentation and distribution of glycans across hSP could help establish molecular environments supporting specific biological activities based on unique ligand capacities. Soluble and particulate fractions of hSP from healthy subjects were analyzed by gel filtration, electrophoresis, ion-exchange chromatography and a solid phase assay with immobilized charge-resolved glycospecies to test their reactivity with plant lectins, carbohydrate-binding antibodies and selected human lectins. Common O- and N-glycosylated species were detected on mixed or overlapped underlying protein scaffolds in both soluble and particulate fractions of hSP. Siaα2,6Gal and N-glycans were concentrated on EVs, whereas Siaα2,3Gal, T and Tn antigens were selectively associated with distinct glycospecies of ASG/mucins. Accessible ligands for the lectins, DC-SIGN and Siglec-9, were detected in all hSP components, but they preferentially bound to EVs glycospecies. Insight into the complexity of hSP glycans as recognition signals under normal physiological conditions could be of interest for regulation and possible modulation of its biological activity, as well as for biomarker potential related to male health.
      Graphical abstract image

      PubDate: 2016-09-24T15:36:38Z
      DOI: 10.1016/j.abb.2016.09.005
      Issue No: Vol. 609 (2016)
       
  • CD147 induces up-regulation of vascular endothelial growth factor in
           U937-derived foam cells through PI3K/AKT pathway
    • Authors: JiaXin Zong; YunTian Li; DaYong Du; Yang Liu; YongJun Yin
      Pages: 31 - 38
      Abstract: Publication date: Available online 9 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): JiaXin Zong, YunTian Li, DaYong Du, Yang Liu, YongJun Yin
      Intraplaque angiogenesis has been recognized as an important risk factor for the rupture of advanced atherosclerotic plaques in recent years. CD147, also called Extracellular Matrix Metalloproteinase Inducer, has been found the ability to promote angiogenesis in many pathological conditions such as cancer diseases and rheumatoid arthritis via the up-regulation of vascular endothelial growth factor (VEGF), a critical mediator of angiogenesis. We investigated whether CD147 would also induce the up-regulation of VEGF in the foam cells formation process and explored the probable signaling pathway. The results showed the expression of CD147 and VEGF was significantly higher in U937-derived foam cells. After CD147 stealth siRNA transfection treatment, the production of VEGF was reduced depended on the inhibition efficiency of CD147 siRNAs.The special signaling pathway inhibitors LY294002, SP600125, SB203580 and U0126 were added to cultures respectively and the results showed LY294002 dose-dependently inhibited the expression of VEGF. The reduction of phospho-Akt was observed in both LY294002 and siRNA groups, suggested that the phosphatidylinositol 3-kinase/Akt pathway may be the probable signaling pathway underlying CD147 induced up-regulation of VEGF in U937-derived foam cells.

      PubDate: 2016-09-10T14:43:56Z
      DOI: 10.1016/j.abb.2016.09.001
      Issue No: Vol. 609 (2016)
       
  • ATF4 regulates arsenic trioxide-mediated NADPH oxidase, ER-mitochondrial
           crosstalk and apoptosis
    • Authors: Ritesh K. Srivastava; Changzhao Li; Aftab Ahmad; Onika Abrams; Marina S. Gorbatyuk; Kevin S. Harrod; Ronald C. Wek; Farrukh Afaq; Mohammad Athar
      Pages: 39 - 50
      Abstract: Publication date: Available online 13 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Ritesh K. Srivastava, Changzhao Li, Aftab Ahmad, Onika Abrams, Marina S. Gorbatyuk, Kevin S. Harrod, Ronald C. Wek, Farrukh Afaq, Mohammad Athar
      Arsenic is a mitochondrial toxin, and its derivatives, such as arsenic trioxide (ATO), can trigger endoplasmic reticulum (ER) and the associated unfolded protein response (UPR). Here, we show that arsenic induction of the UPR triggers ATF4, which is involved in regulating this ER-mitochondrial crosstalk that is important for the molecular pathogenesis of arsenic toxicity. Employing ATF4 +/+ and ATF4 −/− MEFs, we show that ATO induces UPR and impairs mitochondrial integrity in ATF4 +/+ MEF cells which is largely ablated upon loss of ATF4. Following ATO treatment, ATF4 activates NADPH oxidase by promoting assembly of the enzyme components Rac-1/P47phox/P67phox, which generates ROS/superoxides. Furthermore, ATF4 is required for triggering Ca++/calpain/caspase-12-mediated apoptosis following ATO treatment. The IP3R inhibitor attenuates Ca++/calpain-dependent apoptosis, as well as reduces m-ROS and MMP disruption, suggesting that ER-mitochondria crosstalk involves IP3R-regulated Ca++ signaling. Blockade of m-Ca++ entry by inhibiting m-VDAC reduces ATO-mediated UPR in ATF4 +/+ cells. Additionally, ATO treatment leads to p53-regulated mitochondrial apoptosis, where p53 phosphorylation plays a key role. Together, these findings indicate that ATO-mediated apoptosis is regulated by both ER and mitochondria events that are facilitated by ATF4 and the UPR. Thus, we describe novel mechanisms by which ATO orchestrates cytotoxic responses involving interplay of ER and mitochondria.
      Graphical abstract image

      PubDate: 2016-09-15T14:57:26Z
      DOI: 10.1016/j.abb.2016.09.003
      Issue No: Vol. 609 (2016)
       
  • Protein disulfide isomerases: Redox connections in and out of the
           endoplasmic reticulum
    • Authors: Ana Iochabel Soares Moretti; Francisco Rafael Martins Laurindo
      Abstract: Publication date: Available online 24 November 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Ana Iochabel Soares Moretti, Francisco Rafael Martins Laurindo
      Protein disulfide isomerases are thiol oxidoreductase chaperones from thioredoxin superfamily. As redox folding catalysts from the endoplasmic reticulum (ER), their roles in ER-related redox homeostasis and signaling is well-studied. PDIA1 exerts thiol oxidation/reduction and isomerization, plus chaperone effects. Also, substantial evidence indicates that PDIs regulate thiol-disulfide switches in other cell locations such as cell surface and possibly cytosol. Subcellular PDI translocation routes remain unclear and seem Golgi-independent. The list of signaling and structural proteins reportedly regulated by PDIs keeps growing, via thiol switches involving oxidation, reduction and isomerization, S-(de)nytrosylation, (de)glutathyonylation and protein oligomerization. PDIA1 is required for agonist-triggered Nox NADPH oxidase activation and cell migration in vascular cells and macrophages, while PDIA1-dependent cytoskeletal regulation appears a converging pathway. Extracellularly, PDIs crucially regulate thiol redox signaling of thrombosis/platelet activation, e.g., integrins, and PDIA1 supports expansive caliber remodeling during injury repair via matrix/cytoskeletal organization. Some proteins display regulatory PDI-like motifs. PDI effects are orchestrated by expression levels or post-translational modifications. PDI is redox-sensitive, although probably not a mass-effect redox sensor due to kinetic constraints. Rather, the "all-in-one" organization of its peculiar redox/chaperone properties likely provide PDIs with precision and versatility in redox signaling, making them promising therapeutic targets.

      PubDate: 2016-12-01T01:03:36Z
      DOI: 10.1016/j.abb.2016.11.007
       
  • Influence of sequence and lipid type on membrane perturbation by human and
           rat amyloid β-peptide (1–42)
    • Authors: Anne M. Brown; David R. Bevan
      Abstract: Publication date: Available online 21 November 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Anne M. Brown, David R. Bevan
      The hallmark characteristics of plaque formation and neuronal cell death in Alzheimer's disease (AD) are caused principally by the amyloid β-peptide (Aβ). Aβ sequence and lipid composition are essential variables to consider when elucidating the impact of biological membranes on Aβ structure and the effect of Aβ on membrane integrity. Atomistic molecular dynamics simulations testing two Aβ sequences, human and rat Aβ (HAβ and RAβ, respectively), and five lipid types were performed to assess the effect of these variables on membrane perturbation and potential link to AD phenotype differences based on differences in sequence. All metrics agree insomuch that monomeric HAβ and RAβ contribute to membrane perturbation by causing a more rigid, gel-like lipid phase. Differences between HAβ and RAβ binding on degree of membrane perturbation were based on lipid headgroup properties. Cholesterol was found to moderate the amount of perturbation caused by HAβ and RAβ in a model raft membrane. The difference in position of an arginine residue between HAβ and RAβ influenced peptide-membrane interactions and was determined to be the mediating factor in observed differences in lipid affinity and degree of membrane disruption. Overall, this work increases our understanding of the influence of sequence and lipid type on Aβ-membrane interactions and their relationship to AD.
      Graphical abstract image

      PubDate: 2016-11-23T15:43:39Z
      DOI: 10.1016/j.abb.2016.11.006
       
  • Signaling by 4-hydroxy-2-nonenal: Exposure protocols, target selectivity
           and degradation
    • Authors: Hongqiao Zhang; Henry Jay Forman
      Abstract: Publication date: Available online 10 November 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Hongqiao Zhang, Henry Jay Forman
      4-hydroxy-2-nonenal (HNE), a major non-saturated aldehyde product of lipid peroxidation, has been extensively studied as a signaling messenger. In these studies a wide range of HNE concentrations have been used, ranging from the unstressed plasma concentration to far beyond what would be found in actual pathophysiological condition. In addition, accumulating evidence suggest that signaling protein modification by HNE is specific with only those proteins with cysteine, histidine, and lysine residues located in certain sequence or environments adducted by HNE. HNE-signaling is further regulated through the turnover of HNE-signaling protein adducts through proteolytic process that involve proteasomes, lysosomes and autophagy. This review discusses the HNE concentrations and exposure modes used in signaling studies, the selectivity of the HNE-adduction site, and the turnover of signaling protein adducts.

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.11.003
       
  • Long-term inhibition of cyclophilin D results in intracellular
           translocation of calcein AM from mitochondria to lysosomes
    • Authors: Daisuke Shinohe; Asuka Kobayashi; Marina Gotoh; Kotaro Tanaka; Yoshihiro Ohta
      Abstract: Publication date: Available online 15 November 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Daisuke Shinohe, Asuka Kobayashi, Marina Gotoh, Kotaro Tanaka, Yoshihiro Ohta
      Cyclophilin D is a peptidyl-prolyl cis-trans isomerase localized in the mitochondrial matrix. Although its effects on mitochondrial characteristics have been well studied, its relation to the uptake of molecules by mitochondria remains unknown. Here, we demonstrated the effects of cyclophilin D on the intracellular translocation of calcein AM. Following addition of calcein AM to control cells or cells overexpressing wild-type cyclophilin D, calcein fluorescence was observed in mitochondria. However, long-term inhibition of cyclophilin D in these cells altered the localization of calcein fluorescence from mitochondria to lysosomes without changing mitochondrial esterase activity. In addition, depletion of glucose from the medium recovered calcein localization from lysosomes to mitochondria. This is the first demonstration of the effects of cyclophilin D on the intracellular translocation of molecules other than proteins and suggests that cyclophilin D may modify mitochondrial features by inducing the translocation of molecules to the mitochondria through the mechanism associated with cellular energy metabolism.
      Graphical abstract image

      PubDate: 2016-11-16T15:31:43Z
      DOI: 10.1016/j.abb.2016.11.005
       
  • Impact of hypoxia inducible factors on estrogen receptor expression in
           breast cancer cells
    • Authors: Matthias Wolff; Friederike Katharina Kosyna Dunst Wolfgang Jelkmann Reinhard Depping
      Abstract: Publication date: Available online 5 November 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Matthias Wolff, Friederike Katharina Kosyna, Jürgen Dunst, Wolfgang Jelkmann, Reinhard Depping
      In women breast cancer is still the most commonly diagnosed cancer. This type of cancer is classified as a hormone-dependent tumor. Estrogen receptor (ER) expression and functional status contribute to breast cancer development and progression. Another important factor associated with cancer is hypoxia which is defined as the state of reduced oxygen availability in tissues. Intratumoral hypoxia results in the activation of the hypoxia inducible factors (HIFs). HIFs are heterodimeric transcription factors involved in the regulation of many cellular processes, such as angiogenesis, anaerobic metabolism, cell proliferation/survival, and promotion of metastasis. In this study we evaluated the interplay between hypoxia, HIF stabilization and the ER-α/β-ratio in several ER-positive breast cancer cell lines. Hypoxia was shown to inhibit ER expression in ER-positive breast cancer cells. Further experiments using the hypoxia mimetic CoCl2 and HIF-1α knockdown cells indicated that the influence of hypoxia on breast cancer cells involves other pathways than the molecular oxygen sensing pathway. Moreover, we demonstrated that MCF-7 cells in long-term culture lost part of their ability to respond to hypoxic incubation. Understanding the relationships between HIF, ER-α and ER-β expression holds the promise of the development of new therapeutic agents and may provide future advances in prognosis.

      PubDate: 2016-11-09T15:20:08Z
       
  • Cytotoxicity of prion protein-derived cell-penetrating peptides is
           modulated by pH but independent of amyloid formation
    • Authors: Vineeth Mukundan; Christy Maksoudian Maria Vogel Ibrahim Chehade Marios Katsiotis
      Abstract: Publication date: Available online 3 November 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Vineeth Mukundan, Christy Maksoudian, Maria C. Vogel, Ibrahim Chehade, Marios S. Katsiotis, Saeed M. Alhassan, Mazin Magzoub
      Prion diseases are associated with conversion of cellular prion protein (PrPC) into an abnormally folded and infectious scrapie isoform (PrPSc). We previously showed that peptides derived from the unprocessed N-termini of mouse and bovine prion proteins, mPrP1-28 and bPrP1-30, function as cell-penetrating peptides (CPPs), and destabilize model membrane systems, which could explain the infectivity and toxicity of prion diseases. However, subsequent studies revealed that treatment with mPrP1-28 or bPrP1-30 significantly reduce PrPSc levels in prion-infected cells. To explain these seemingly contradictory results, we correlated the aggregation, membrane perturbation and cytotoxicity of the peptides with their cellular uptake and intracellular localization. Although the peptides have a similar primary sequence, mPrP1-28 is amyloidogenic, whereas bPrP1-30 forms smaller oligomeric or non-fibrillar aggregates. Surprisingly, bPrP1-30 induces much higher cytotoxicity than mPrP1-28, indicating that amyloid formation and toxicity are independent. The toxicity is correlated with prolonged residence at the plasma membrane and membrane perturbation. Both ordered aggregation and toxicity of the peptides are inhibited by low pH. Under non-toxic conditions, the peptides are internalized by lipid-raft dependent macropinocytosis and localize to acidic lysosomal compartments. Our results shed light on the antiprion mechanism of the prion protein-derived CPPs and identify a potential site for PrPSc formation.

      PubDate: 2016-11-09T15:20:08Z
       
  • 13C kinetic isotope effects on the reaction of a flavin amine oxidase
           determined from whole molecule isotope effects
    • Authors: José R. Tormos; Marina B. Suarez; Paul F. Fitzpatrick
      Abstract: Publication date: Available online 1 November 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): José R. Tormos, Marina B. Suarez, Paul F. Fitzpatrick
      A large number of flavoproteins catalyze the oxidation of amines. Because of the importance of these enzymes in metabolism, their mechanisms have previously been studied using deuterium, nitrogen, and solvent isotope effects. While these results have been valuable for computational studies to distinguish among proposed mechanisms, a measure of the change at the reacting carbon has been lacking. We describe here the measurement of a 13C kinetic isotope effect for a representative amine oxidase, polyamine oxidase. The isotope effect was determined by analysis of the isotopic composition of the unlabeled substrate, N, N’-dibenzyl-1,4-diaminopropane, to obtain a pH-independent value of 1.025. The availability of a 13C isotope effect for flavoprotein-catalyzed amine oxidation provides the first measure of the change in bond order at the carbon involved in this carbon-hydrogen bond cleavage and will be of value to understanding the transition state structure for this class of enzymes.
      Graphical abstract image

      PubDate: 2016-11-02T14:49:35Z
      DOI: 10.1016/j.abb.2016.10.018
       
  • Probing the orientation of inhibitor and epoxy-eicosatrienoic acid binding
           in the active site of soluble epoxide hydrolase
    • Authors: Kin Sing Stephen Lee; Niel M. Henriksen; Connie J. Ng; Jun Yang; Weitao Jia; Christophe Morisseau; Armann Andaya; Michael K. Gilson; Bruce D. Hammock
      Abstract: Publication date: Available online 29 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Kin Sing Stephen Lee, Niel M. Henriksen, Connie J. Ng, Jun Yang, Weitao Jia, Christophe Morisseau, Armann Andaya, Michael K. Gilson, Bruce D. Hammock
      Soluble epoxide hydrolase (sEH) is an important therapeutic target of many diseases, such as chronic obstructive pulmonary disease (COPD) and diabetic neuropathic pain. It acts by hydrolyzing and thus regulating specific bioactive long chain polyunsaturated fatty acid epoxides (lcPUFA), like epoxyeicosatrienoic acids (EETs). To better predict which epoxides could be hydrolyzed by sEH, one needs to dissect the important factors and structural requirements that govern the binding of the substrates to sEH. This knowledge allows further exploration of the physiological role played by sEH. Unfortunately, a crystal structure of sEH with a substrate bound has not yet been reported. In this report, new photoaffinity mimics of a sEH inhibitor and EET were prepared and used in combination with peptide sequencing and computational modeling, to identify the binding orientation of different regioisomers and enantiomers of EETs into the catalytic cavity of sEH. Results indicate that the stereochemistry of the epoxide plays a crucial role in dictating the binding orientation of the substrate.
      Graphical abstract image

      PubDate: 2016-11-02T14:49:35Z
      DOI: 10.1016/j.abb.2016.10.017
       
  • An insight into fusion technology aiding efficient recombinant protein
           production for functional proteomics
    • Authors: Dinesh K. Yadav; Neelam Yadav; Sarika Yadav; Shafiul Haque; Narendra Tuteja
      Abstract: Publication date: Available online 19 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Dinesh K. Yadav, Neelam Yadav, Sarika Yadav, Shafiul Haque, Narendra Tuteja
      Advancements in peptide fusion technologies to maximize the protein production has taken a big leap to fulfill the demands of post-genomics era targeting elucidation of structure/function of the proteome and its therapeutic applications, by over-expression in heterologous expression systems. Despite being most preferred protein expression system armed with variety of cardinal fusion tags, expression of the functionally active recombinant protein in E. coli remains plagued. The present review critically analyses the aptness of well-characterized fusion tags utilized for over-expression of recombinant proteins with improved solubility and their compatibility with downstream purification procedures. The combinatorial tandem affinity strategies have shown to provide more versatile options. Solubility decreasing fusion tags have proved to facilitate the overproduction of antimicrobial peptides. Efficient removal of fusion tags prior to final usage is of utmost importance and has been summarized discussing the efficiency of various enzymatic and chemical methods of tag removal. Unfortunately, no single fusion tag works as a magic bullet to completely fulfill the requirements of protein expression and purification in active form. The information provided might help in selection and development of a successful protocol for efficient recombinant protein production for functional proteomics.

      PubDate: 2016-10-27T22:46:44Z
      DOI: 10.1016/j.abb.2016.10.012
       
  • Neutrophils recruited to the myocardium after acute experimental
           myocardial infarct generate hypochlorous acid that oxidizes cardiac
           myoglobin
    • Authors: Xiao Suo Wang; Hyun Bo Kim; Andrea Szuchman-Sapir; Aisling McMahon; Joanne M. Dennis; Paul K. Witting
      Abstract: Publication date: Available online 24 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Xiao Suo Wang, Hyun Bo Kim, Andrea Szuchman-Sapir, Aisling McMahon, Joanne M. Dennis, Paul K. Witting
      Myocardial inflammation following acute myocardial infarct (AMI) is associated with risk of congestive heart failure. Pro-inflammatory neutrophils were recruited to the damaged myocardium 24 h after permanent coronary ligation in rats to induce AMI as judged by the presence of immune-positive myeloperoxidase (MPO) in the tissues; MPO generates the oxidant hypochlorous acid (HOCl). Neutrophils were absent in hearts from Control (untreated) and surgical Sham. Similarly, rats exposed to 1 h coronary ligation (Ischemia) showed no neutrophil infiltrate. Concomitantly, MPO activity increased in left ventricular (LV) homogenates prepared from the AMI group and this was inhibited by paracetamol and the nitroxide TEMPO. The same LV-homogenates showed increased 3-chlorotyrosine/tyrosine ratios (biomarker for MPO-activity). Combined 2D gel/Western blot indicated cardiac myoglobin (Mb) was modified after AMI. Subsequent MALDI-TOF and LC-MS/MS analysis of isolated protein spots revealed increased Mb oxidation in hearts from the AMI group relative to Control, Sham and Ischemia groups. Peptide mass mapping revealed oxidation of Met9 and Met132 to the corresponding sulfoxides yet Cys67 remained unmodified. Therefore, neutrophil-generated HOCl can oxidize cardiac Mb after AMI and this may impact on its function within the affected myocardium: oxidized Mb maybe a useful marker of myocardial inflammation.
      Graphical abstract image

      PubDate: 2016-10-27T22:46:44Z
      DOI: 10.1016/j.abb.2016.10.013
       
  • Repositioning nordihydroguaiaretic acid as a potent inhibitor of systemic
           amyloidosis and associated cellular toxicity
    • Authors: Saima Nusrat; Nida Zaidi; Masihuz Zaman; Sehbanul Islam; Mohammad Rehan Ajmal; Mohammad Khursheed Siddiqi; Manas Kumar Santra; Rizwan Hasan Khan
      Abstract: Publication date: Available online 24 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Saima Nusrat, Nida Zaidi, Masihuz Zaman, Sehbanul Islam, Mohammad Rehan Ajmal, Mohammad Khursheed Siddiqi, Manas Kumar Santra, Rizwan Hasan Khan
      Although the cure of amyloid related neurodegenerative diseases, non-neuropathic amyloidogenic diseases and non-neuropathic systemic amyloidosis are appealing energetic research attempts, beneficial medication is still to be discovered. There is a need to explore intensely stable therapeutic compounds, potent enough to restrict, disrupt or wipe out such toxic aggregates. We had performed a comprehensive biophysical, computational and cell based assay, that shows Nordihydroguaiaretic acid (NA) not only significantly inhibits heat induced hen egg white lysozyme (HEWL) fibrillation but also disaggregates preformed HEWL fibrils and reduces the cytoxicity of amyloid fibrils as well as disaggregated fibrillar species. The inhibitory potency of NA was determined by an IC50 of 26.3 μM. NA was also found to effectively inhibit human lysozyme (HL) fibrillation. NA interferes in the amyloid fibrillogenesis process by interacting hydrophobically with the amino acid residues found in highly prone amyloid fibril forming region of HEWL as explicated by molecular docking results. The results recommend NA as a probable neuroprotective and promising inhibitor for the therapeutic advancement prospective against amyloid related diseases.
      Graphical abstract image

      PubDate: 2016-10-27T22:46:44Z
      DOI: 10.1016/j.abb.2016.10.014
       
  • Reciprocal regulation of acetyl-CoA carboxylase 1 and senescence in human
           fibroblasts involves oxidant mediated p38 MAPK activation
    • Authors: Inés Marmisolle; Jennyfer Martínez; Jie Liu; Mauricio Mastrogiovanni; María M. Fergusson; Ilsa I. Rovira; Laura Castro; Andrés Trostchansky; María Moreno; Liu Cao; Toren Finkel; Celia Quijano
      Abstract: Publication date: Available online 27 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Inés Marmisolle, Jennyfer Martínez, Jie Liu, Mauricio Mastrogiovanni, María M. Fergusson, Ilsa I. Rovira, Laura Castro, Andrés Trostchansky, María Moreno, Liu Cao, Toren Finkel, Celia Quijano
      We sought to explore the fate of the fatty acid synthesis pathway in human fibroblasts exposed to DNA damaging agents capable of inducing senescence, a state of irreversible growth arrest. Induction of premature senescence by doxorubicin or hydrogen peroxide led to a decrease in protein and mRNA levels of acetyl-CoA carboxylase 1 (ACC1), the enzyme that catalyzes the rate-limiting step in fatty-acid biosynthesis. ACC1 decay accompanied the activation of the DNA damage response (DDR), and resulted in decreased lipid synthesis. A reduction in protein and mRNA levels of ACC1 and in lipid synthesis was also observed in human primary fibroblasts that underwent replicative senescence. We also explored the consequences of inhibiting fatty acid synthesis in proliferating non-transformed cells. Using shRNA technology, we knocked down ACC1 in human fibroblasts. Interestingly, this metabolic perturbation was sufficient to arrest proliferation and trigger the appearance of several markers of the DDR and increase senescence associated β-galactosidase activity. Reactive oxygen species and p38 mitogen activated protein kinase phosphorylation participated in the induction of senescence. Similar results were obtained upon silencing of fatty acid synthase (FAS) expression. Together our results point towards a tight coordination of fatty acid synthesis and cell proliferation in human fibroblasts.
      Graphical abstract image

      PubDate: 2016-10-27T22:46:44Z
      DOI: 10.1016/j.abb.2016.10.016
       
  • Development of the first internally-quenched fluorescent substrates of
           human cathepsin C: The application in the enzyme detection in biological
           samples
    • Authors: Monika Łęgowska; Yveline Hamon; Anna Wojtysiak; Renata Grzywa; Marcin Sieńczyk; Timo Burster; Brice Korkmaz; Adam Lesner
      Abstract: Publication date: Available online 13 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Monika Łęgowska, Yveline Hamon, Anna Wojtysiak, Renata Grzywa, Marcin Sieńczyk, Timo Burster, Brice Korkmaz, Adam Lesner
      Cathepsin C is a wildly expressed cysteine exopeptidase that is mostly recognized for the activation of the granule-associated proinflammatory serine proteases in neutrophils, cytotoxic T lymphocytes and mast cells. It has been shown that the enzyme can be secreted extracellularly; however, its occurrence in human bodily fluids/physiological samples has not been thoroughly studied. In the course of this study, the first fluorescence resonance energy transfer peptides for the measurement of the activity of human cathepsin C were designed and synthesized. Two series of tetra- and pentapeptide substrates enabled the detailed S′ specificity study of cathepsin C, which has been examined for the first time. The extensive enzymatic studies of the obtained compounds resulted in the selection of the highly specific and selective substrate Thi-Ala(Mca)-Ser-Gly-Tyr(3-NO2)-NH2, which was successfully employed for the detection of cathepsin C activity in complex biological samples such as cell lysates, urine and bronchoalveolar lavage fluids. Molecular docking of the selected substrate was performed in order to better understand the binding mode of the substrates in the active site of cathepsin C.

      PubDate: 2016-10-19T12:26:14Z
      DOI: 10.1016/j.abb.2016.10.007
       
  • Ligand binding phenomena that pertain to the metabolic function of
           renalase
    • Authors: Brett A. Beaupre; Joseph V. Roman; Matthew R. Hoag; Kathleen M. Meneely; Nicholas R. Silvaggi; Audrey L. Lamb; Graham R. Moran
      Abstract: Publication date: Available online 18 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Brett A. Beaupre, Joseph V. Roman, Matthew R. Hoag, Kathleen M. Meneely, Nicholas R. Silvaggi, Audrey L. Lamb, Graham R. Moran
      Renalase catalyzes the oxidation of isomers of β-NAD(P)H that carry the hydride in the 2 or 6 positions of the nicotinamide base to form β-NAD(P)+. This activity is thought to alleviate inhibition of multiple β-NAD(P)-dependent enzymes of primary and secondary metabolism by these isomers. Here we present evidence for a variety of ligand binding phenomena relevant to the function of renalase. We offer evidence of the potential for primary metabolism inhibition with structures of malate dehydrogenase and lactate dehydrogenase bound to the 6-dihydroNAD isomer. The previously observed preference of renalase from Pseudomonas for NAD-derived substrates over those derived from NADP is accounted for by the structure of the enzyme in complex with NADPH. We also show that nicotinamide nucleosides and mononucloetides reduced in the 2- and 6-positions are renalase substrates, but bind weakly. A seven-fold enhancement of acquisition (kred/K d) for 6-dihydronicotinamide riboside was observed for human renalase in the presence of ADP. However, generally the addition of complement ligands, ADP for mononucloetide or AMP for nucleoside substrates, did not enhance the reductive half-reaction. Non-substrate nicotinamide nucleosides or nucleotides bind weakly suggesting that only β-NADH and β-NADPH compete with dinucleotide substrates for access to the active site.
      Graphical abstract image

      PubDate: 2016-10-19T12:26:14Z
      DOI: 10.1016/j.abb.2016.10.011
       
  • Photoacoustic calorimetry studies of CO photo-dissociation from
           chloramine-T modified horse heart cytochrome-c
    • Authors: Tarah A. Word; Randy W. Larsen
      Abstract: Publication date: Available online 4 October 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Tarah A. Word, Randy W. Larsen
      Treatment of horse heart Cytochrome-c (Cc) with N-chloro-4-toluosulfonamide (Chloramine-t, CT) results in the oxidation of methionine (Met) residues to the corresponding sulfoxide including the distal heme ligand, Met80. The resulting Fe-sulfoxide coordination is sufficiently labile in the ferrous form to be displaced by gaseous ligands, including CO. Photolysis of the CO-CT-Cc complex provides an opportunity to examine ligand binding dynamics that are associated with a relatively rigid distal heme pocket. In this work, photoacoustic calorimetry (PAC) was utilized to obtain the kinetics as well as enthalpy and molar volume changes subsequent to CO photo-dissociation from CO-CT-Cc. Previous photolysis studies of CO-CT-Cc have led to a proposed model for ligand recombination in which the Met80-sulfoxide and CO recombine with the heme on relatively slow timescales (50 μs and ∼500 μs, respectively). The PAC data presented here reveals two additional kinetic phases with lifetimes of <20 ns and 534 ± 75 ns. The fast phase (<20 ns) is associated with an ΔH of 44 ± 5 kcal mol−1 and ΔV of −0.5 ± 0.5 mL mol−1, whereas the slower phase (534 ns) is associated with a small ΔH of 2 ± 3 kcal mol−1 and ΔV of 1 ± 0.5 mL mol−1.
      Graphical abstract image

      PubDate: 2016-10-06T16:07:59Z
      DOI: 10.1016/j.abb.2016.10.001
       
  • Physico-chemical characteristics and primary structure of an
           affinity-purified α-D-galactose-specific, jacalin-related lectin from the
           latex of mulberry (Morus indica)
    • Authors: Debparna Datta; Gottfried Pohlentz; Mona Schulte; Mathias Kaiser; Francisco M. Goycoolea; Johannes Müthing; Michael Mormann; Musti J. Swamy
      Abstract: Publication date: Available online 21 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Debparna Datta, Gottfried Pohlentz, Mona Schulte, Mathias Kaiser, Francisco M. Goycoolea, Johannes Müthing, Michael Mormann, Musti J. Swamy
      An α-D-galactose specific lectin belonging to the family of jacalin-related lectins (JRL) has been purified by affinity chromatography on cross-linked guar-gum. Mass spectrometric data suggested that the protein harbors two chains like all the members of galactose-specific jacalin-related lectins (gJRL). De novo sequencing of proteolytic peptides demonstrated that the heavier chain consists of 133 amino acids and the lighter chain comprises of 21 or 24 amino acids. The heavier chain contains one N-glycosylation site (Asn47) occupied with either pauci-mannose type [GlcNAc2(Fuc)Man3(Xyl)] or complex type [GlcNAc2(Fuc)Man3(Xyl)GlcNAc(Fuc)Gal] N-glycans. Circular dichroism spectroscopy indicated that the secondary structure of the lectin is predominantly made up of β-sheets, and differential scanning calorimetry revealed a thermal denaturation temperature of 77.6 °C. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) cell viability assays on MCF-7 and MDCK cells showed that the lectin is highly cytotoxic towards both cell lines when dosed at micromolar concentrations, suggesting that it may play a role in the defense mechanism of the plant.

      PubDate: 2016-09-21T15:25:50Z
      DOI: 10.1016/j.abb.2016.09.009
       
  • The propensity for tropomyosin twisting in the presence and absence of
           F-actin
    • Authors: Michael J. Rynkiewicz; Stefan Fischer; William Lehman
      Abstract: Publication date: Available online 20 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Michael J. Rynkiewicz, Stefan Fischer, William Lehman
      A canonical model of muscle α-tropomyosin (Tpm1.1), based on molecular-mechanics and electron microscopy of different contractile states, shows that the two-stranded coiled-coiled is pre-bent to present a specific molecular-face to the F-actin filament. This conformation is thought to facilitate both filament assembly and tropomyosin sliding across actin to modulate myosin-binding. However, to bind effectively to actin filaments, the 42 nm-long tropomyosin coiled-coil is not strictly canonical. Here, the mid-region of tropomyosin twists an additional ∼20° in order to better match the F-actin helix. In addition, the N- and C-terminal regions of tropomyosin polymerize head-to-tail to form continuous super-helical cables. In this case, 9 to 10 residue-long overlapping domains between adjacent molecules untwist relative to each other to accommodate orthogonal interactions between chains in the junctional four-helix nexus. Extensive molecular dynamics simulations show that the twisting and untwisting motions of tropomyosin vary appreciably along tropomyosin length, and in particular that substantial terminal domain winding and unwinding occurs whether tropomyosin is bound to F-actin or not. The local and regional twisting and untwisting do not appear to proceed in a concerted fashion, resembling more of a “wringing-type” behavior rather than a rotation.
      Graphical abstract image

      PubDate: 2016-09-21T15:25:50Z
      DOI: 10.1016/j.abb.2016.09.008
       
  • RKIP suppresses the proliferation and metastasis of breast cancer cell
           lines through up-regulation of miR-185 targeting HMGA2
    • Authors: Qiongyan Zou; Haijun Wu; Fenfen Fu; Wenjun Yi; Lei Pei; Meirong Zhou
      Abstract: Publication date: Available online 17 September 2016
      Source:Archives of Biochemistry and Biophysics
      Author(s): Qiongyan Zou, Haijun Wu, Fenfen Fu, Wenjun Yi, Lei Pei, Meirong Zhou
      Raf-1 kinase inhibitor protein (RKIP) is a tumor and metastasis suppressor in cancer cells. MicroRNAs (miRNAs) have been suggested to play a vital role in tumor initiation and progression by negatively regulating oncogenes and tumor suppressors. Quite recently, studies have identified some miRNAs operating to promote or suppress tumor invasion or metastasis via regulating metastasis-related genes, providing potential therapeutic targets on anti-metastasis strategy. In this study, we found the expression of RKIP and miR-185 in breast cancer tissues was significantly lower than that of in normal breast tissues. Over-expression of RKIP up-regulated miR-185 expression, inhibited breast cancer cell growth and invasion, and inhibited miR-185 target gene High-mobility group AT-hook 2 (HMGA2). HMGA2 is encoded by HMGA2 gene, which encodes a protein that belongs to the non-histone chromosomal high-mobility group (HMG) protein family. Moreover, RKIP knockdown attenuated the inhibition of breast cancer cell invasion and the expression of HMGA2 by miR-185. Forced HMGA2 overexpression could partly restore the inhibitory effect of miR-185 on breast cancer cell growth and invasion. Our findings newly described RKIP/miR-185 to HMGA2 link and provided a potential mechanism for breast cancer cell growth and invasion. It may illustrate the potential therapeutic utility of signaling pathway signatures.

      PubDate: 2016-09-21T15:25:50Z
      DOI: 10.1016/j.abb.2016.09.007
       
 
 
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