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Fisheries and Aquatic Sciences     Open Access   (Followers: 3, SJR: 0.199, CiteScore: 0)
Cancers of the Head & Neck     Open Access   (Followers: 3)
Implementation Science Communications     Open Access   (Followers: 3)
Clinical and Translational Allergy     Open Access   (Followers: 3, SJR: 1.425, CiteScore: 4)
J. of Clinical Movement Disorders     Open Access   (Followers: 3)
Advances in Rheumatology     Open Access   (Followers: 3)
J. of Animal Science and Technology     Open Access   (Followers: 3)
Flavour     Open Access   (Followers: 3)
Biomarker Research     Open Access   (Followers: 3)
Cancer Imaging     Open Access   (Followers: 3, SJR: 1.012, CiteScore: 3)
Asthma Research and Practice     Open Access   (Followers: 2)
Inflammation and Regeneration     Open Access   (Followers: 2)
Intl. J. of Retina and Vitreous     Open Access   (Followers: 2)
Public Health Reviews     Open Access   (Followers: 2, SJR: 0.454, CiteScore: 1)
Biology of Sex Differences     Open Access   (Followers: 2, SJR: 1.902, CiteScore: 4)
Tropical Diseases, Travel Medicine and Vaccines     Open Access   (Followers: 2)
J. of Angiogenesis Research     Open Access   (Followers: 2)
Fertility Research and Practice     Open Access   (Followers: 2)
Urban Transformations     Open Access   (Followers: 2)
J. of Biomedical Semantics     Open Access   (Followers: 2, SJR: 0.952, CiteScore: 2)
CABI Agriculture and Bioscience     Open Access   (Followers: 2)
BMC Materials     Open Access   (Followers: 2)
One Health Outlook     Open Access   (Followers: 2)
NeuroCommons     Open Access   (Followers: 2)
Signals     Open Access   (Followers: 2)
Contraception and Reproductive Medicine     Open Access   (Followers: 2)
Animal Biotelemetry     Open Access   (Followers: 2, SJR: 1.067, CiteScore: 2)
J. of Inflammation     Open Access   (Followers: 2, SJR: 1.101, CiteScore: 3)
J. of Neuroinflammation     Open Access   (Followers: 2, SJR: 2.336, CiteScore: 5)
Neural Development     Open Access   (Followers: 2, SJR: 1.821, CiteScore: 2)
Chinese Medicine     Open Access   (Followers: 2, SJR: 0.57, CiteScore: 2)
Fluids and Barriers of the CNS     Open Access   (Followers: 2, SJR: 2.054, CiteScore: 5)
Cell Communication and Signaling     Open Access   (Followers: 2, SJR: 2.211, CiteScore: 4)
Cancer Nanotechnology     Open Access   (Followers: 2, SJR: 1.168, CiteScore: 4)
Particle and Fibre Toxicology     Open Access   (Followers: 2, SJR: 2.253, CiteScore: 8)
Molecular Neurodegeneration     Open Access   (Followers: 2, SJR: 3.418, CiteScore: 7)
Italian J. of Pediatrics     Open Access   (Followers: 2, SJR: 0.685, CiteScore: 2)
Plant Methods     Open Access   (Followers: 2, SJR: 1.885, CiteScore: 4)
Hereditary Cancer in Clinical Practice     Open Access   (Followers: 2, SJR: 0.848, CiteScore: 2)
BMC Proceedings     Full-text available via subscription   (Followers: 2, SJR: 0.302, CiteScore: 1)
J. of Experimental & Clinical Cancer Research     Open Access   (Followers: 2, SJR: 2, CiteScore: 6)
Reproductive Health     Open Access   (Followers: 2, SJR: 1.228, CiteScore: 2)
World J. of Surgical Oncology     Open Access   (Followers: 2, SJR: 0.688, CiteScore: 2)
Canine Genetics and Epidemiology     Open Access   (Followers: 1)
Eye and Vision     Open Access   (Followers: 1)
Acta Neuropathologica Communications     Open Access   (Followers: 1, SJR: 2.683, CiteScore: 5)
Cerebellum & Ataxias     Open Access   (Followers: 1)
Translational Neurodegeneration     Open Access   (Followers: 1, SJR: 1.901, CiteScore: 5)
Pilot and Feasibility Studies     Open Access   (Followers: 1)
J. of Environmental Health Science & Engineering     Open Access   (Followers: 1, SJR: 0.802, CiteScore: 3)
Infectious Diseases of Poverty     Open Access   (Followers: 1, SJR: 1.212, CiteScore: 3)
Cancer Convergence     Open Access   (Followers: 1)
BMC Zoology     Open Access   (Followers: 1)
Bioelectronic Medicine     Open Access   (Followers: 1)
European J. of Medical Research     Open Access   (Followers: 1, SJR: 0.55, CiteScore: 1)
Scoliosis and Spinal Disorders     Open Access   (Followers: 1, SJR: 0.843, CiteScore: 2)
Women's Midlife Health     Open Access   (Followers: 1)
Genes and Environment     Open Access   (Followers: 1, SJR: 0.516, CiteScore: 1)
Gynecologic Oncology Research and Practice     Open Access   (Followers: 1)
COPD Research and Practice     Open Access   (Followers: 1, SJR: 0.755, CiteScore: 2)
Biological Research     Open Access   (Followers: 1, SJR: 0.654, CiteScore: 2)
J. of Venomous Animals and Toxins including Tropical Diseases     Open Access   (Followers: 1, SJR: 0.573, CiteScore: 2)
Orphanet J. of Rare Diseases     Open Access   (Followers: 1, SJR: 1.413, CiteScore: 3)
Skeletal Muscle     Open Access   (Followers: 1, SJR: 2.32, CiteScore: 4)
J. of Medical Case Reports     Open Access   (Followers: 1, SJR: 0.331, CiteScore: 1)
Head & Face Medicine     Open Access   (Followers: 1, SJR: 0.62, CiteScore: 2)
BMC Ear, Nose and Throat Disorders     Open Access   (Followers: 1, SJR: 0.653, CiteScore: 2)
Cell Division     Open Access   (Followers: 1, SJR: 2.445, CiteScore: 4)
Respiratory Research     Open Access   (Followers: 1, SJR: 1.644, CiteScore: 4)
Proteome Science     Open Access   (Followers: 1, SJR: 0.792, CiteScore: 2)
Theoretical Biology and Medical Modelling     Open Access   (Followers: 1, SJR: 0.783, CiteScore: 2)
Hereditas     Open Access   (Followers: 1, SJR: 0.278, CiteScore: 1)
World Allergy Organization J.     Open Access   (Followers: 1, SJR: 1.936, CiteScore: 6)
Investigative Genetics     Open Access   (Followers: 1, SJR: 1.809, CiteScore: 3)
J. of Cardiovascular Magnetic Resonance     Open Access   (Followers: 1, SJR: 2.292, CiteScore: 5)
Molecular Cytogenetics     Open Access   (Followers: 1, SJR: 0.623, CiteScore: 1)
Thyroid Research     Open Access   (Followers: 1, SJR: 0.329, CiteScore: 1)
Phytopathology Research     Open Access  
Measurement Instruments for the Social Sciences     Open Access  
BMC Energy     Open Access  
Sustainable Earth     Open Access  
BMC Biomedical Engineering     Open Access  
BMC Chemical Engineering     Open Access  
ExRNA     Open Access  
J. of Cotton Research     Open Access  
Biomedical Dermatology     Open Access  
Cancer Communications     Open Access  
Diagnostic and Prognostic Research     Open Access  
Porcine Health Management     Open Access  
Neurovascular Imaging     Open Access  
NeuroMetals     Open Access  
Chinese Neurosurgical J.     Open Access  
Cardio-Oncology     Open Access  
Neuropsychiatric Electrophysiology     Open Access  
Research Involvement and Engagement     Open Access  
J. of Biological Research - Thessaloniki     Open Access   (SJR: 0.32, CiteScore: 2)
Israel J. of Health Policy Research     Open Access   (SJR: 0.488, CiteScore: 1)
Vascular Cell     Open Access   (SJR: 1.349, CiteScore: 4)
Environmental Microbiome     Open Access   (SJR: 0.768, CiteScore: 2)
Mobile DNA     Open Access   (SJR: 3.783, CiteScore: 5)
J. of Neurodevelopmental Disorders     Open Access   (SJR: 1.71, CiteScore: 4)
Biological Procedures Online     Open Access   (SJR: 1.352, CiteScore: 4)
Basic and Clinical Andrology     Open Access   (SJR: 0.564, CiteScore: 2)
PMC Biophysics     Open Access  
Fibrogenesis & Tissue Repair     Open Access   (SJR: 1.531, CiteScore: 4)
J. of Ovarian Research     Open Access   (SJR: 1.008, CiteScore: 3)
Source Code for Biology and Medicine     Open Access   (SJR: 0.784, CiteScore: 2)
Retrovirology     Open Access   (SJR: 1.855, CiteScore: 3)
Lipids in Health and Disease     Open Access   (SJR: 0.915, CiteScore: 2)
J. of Negative Results in BioMedicine     Open Access   (SJR: 0.483, CiteScore: 1)
J. of Ethnobiology and Ethnomedicine     Open Access   (SJR: 0.693, CiteScore: 3)
Infectious Agents and Cancer     Open Access   (SJR: 0.855, CiteScore: 2)
Harm Reduction J.     Open Access   (SJR: 1.445, CiteScore: 3)

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Cell Division
Journal Prestige (SJR): 2.445
Citation Impact (citeScore): 4
Number of Followers: 1  

  This is an Open Access Journal Open Access journal
ISSN (Print) 1747-1028
Published by BMC (Biomed Central) Homepage  [313 journals]
  • Eg5 orchestrates porcine oocyte maturational progression by maintaining
           meiotic organelle arrangement

    • Abstract: Background Kinesin superfamily proteins are microtubule-based molecular motors essential for the intracellular transport of various cargos, including organelles, proteins, and RNAs. However, their exact roles during mammalian oocyte meiosis have not been fully clarified. Results Herein, we investigated the critical events during porcine oocyte meiotic maturation with the treatment of Eg5-specific inhibitor monastrol. We found that Eg5 inhibition resulted in oocyte meiotic failure by displaying the poor expansion of cumulus cells and reduced rate of polar body extrusion. In the meantime, the spindle assembly and chromosome alignment were compromised, accompanied by the decreased level of acetylated α-tubulin, indicative of less stable microtubules. Impaired actin dynamics and mitochondria integrity were also observed in Eg5-inhibited oocytes. Additionally, inhibition of Eg5 caused the abnormal distribution of cortical granules and ovastacin, a cortical granule component, potentially leading to the fertilization failure. Conclusions Our findings reveal that Eg5 possesses an important function in porcine oocyte meiotic progression by regulating the organelle dynamics and arrangement.
      PubDate: 2018-05-24
  • Protein arginine methylation: an emerging regulator of the cell cycle

    • Abstract: Abstract Protein arginine methylation is a common post-translational modification where a methyl group is added onto arginine residues of a protein to alter detection by its binding partners or regulate its activity. It is known to be involved in many biological processes, such as regulation of signal transduction, transcription, facilitation of protein–protein interactions, RNA splicing and transport. The enzymes responsible for arginine methylation, protein arginine methyltransferases (PRMTs), have been shown to methylate or associate with important regulatory proteins of the cell cycle and DNA damage repair pathways, such as cyclin D1, p53, p21 and the retinoblastoma protein. Overexpression of PRMTs resulting in aberrant methylation patterns in cancers often correlates with poor recovery prognosis. This indicates that protein arginine methylation is also an important regulator of the cell cycle, and consequently a target for cancer regulation. The effect of protein arginine methylation on the cell cycle and how this emerging key player of cell cycle regulation may be used in therapeutic strategies for cancer are the focus of this review.
      PubDate: 2018-03-20
  • Subunits of human condensins are potential therapeutic targets for cancers

    • Abstract: Abstract The main role of condensins is to regulate chromosome condensation and segregation during cell cycles. Recently, it has been suggested in the literatures that subunits of condensin I and condensin II are involved in some human cancers. This paper will first briefly discuss discoveries of human condensins, their components and structures, and their multiple cellular functions. This will be followed by reviews of most recent studies on subunits of human condensins and their dysregulations or mutations in human cancers. It can be concluded that many of these subunits have potentials to be novel targets for cancer therapies. However, hCAP-D2, a subunit of human condensin I, has not been directly documented to be associated with any human cancers to date. This review hypothesizes that hCAP-D2 can also be a potential therapeutic target for human cancers, and therefore that all subunits of human condensins are potential therapeutic targets for human cancers.
      PubDate: 2018-02-20
  • Phasing in on the cell cycle

    • Abstract: Abstract Just like all matter, proteins can also switch between gas, liquid and solid phases. Protein phase transition has claimed the spotlight in recent years as a novel way of how cells compartmentalize and regulate biochemical reactions. Moreover, this discovery has provided a new framework for the study of membrane-less organelle biogenesis and protein aggregation in neurodegenerative disorders. We now argue that this framework could be useful in the study of cell cycle regulation and cancer. Based on our work on phase transitions of arginine-rich proteins in neurodegeneration, via combining mass spectroscopy with bioinformatics analyses, we found that also numerous proteins involved in the regulation of the cell cycle can undergo protein phase separation. Indeed, several proteins whose function affects the cell cycle or are associated with cancer, have been recently found to phase separate from the test tube to cells. Investigating the role of this process for cell cycle proteins and understanding its molecular underpinnings will provide pivotal insights into the biology of cell cycle progression and cancer.
      PubDate: 2018-01-25
  • The emerging roles of CDK12 in tumorigenesis

    • Abstract: Abstract Cyclin-dependent kinases (CDKs) are key regulators of both cell cycle progression and transcription. Since dysregulation of CDKs is a frequently occurring event driving tumorigenesis, CDKs have been tested extensively as targets for cancer therapy. Cyclin-dependent kinase 12 (CDK12) is a transcription-associated kinase which participates in various cellular processes, including DNA damage response, development and cellular differentiation, as well as splicing and pre-mRNA processing. CDK12 mutations and amplification have been recently reported in different types of malignancies, including loss-of-function mutations in high-grade serous ovarian carcinomas, and that has led to assumption that CDK12 is a tumor suppressor. On the contrary, CDK12 overexpression in other tumors suggests the possibility that CDK12 has oncogenic properties, similarly to other transcription-associated kinases. In this review, we discuss current knowledge concerning the role of CDK12 in ovarian and breast tumorigenesis and the potential for chemical inhibitors of CDK12 in future cancer treatment.
      PubDate: 2017-10-27
  • Proteins associated with the doubling time of the NCI-60 cancer cell lines

    • Abstract: Abstract The varied nature of human cancers is recapitulated, at least to some extent, in the diverse NCI-60 panel of human cancer cell lines. Here, I used a basic, continuous variable of proliferating cells, their doubling time, to stratify the proteome across the NCI-60 cell lines. Among >7000 proteins quantified in the NCI-60 panel previously, the levels of 84 proteins increase in cells that proliferate slowly. This set overlapped with the hallmark molecular signature “epithelial-mesenchymal transition (EMT)” (p value = 1.1E−07). Conversely, the levels of 105 proteins increased in cells that proliferate faster and overlapped with the molecular signatures for “MYC targets V1” (p value = 3.8E−38) and “E2F targets” (p value = 2.4E−34). These data for the first time identify proteins whose levels are dynamically associated with doubling time, but not necessarily with cancer type origins, and argue for the incorporation of doubling time measurements in cell line-based profiling studies.
      PubDate: 2017-08-29
  • Erratum to: Rpl22 is required for IME1 mRNA translation and meiotic
           induction in S. cerevisiae

    • PubDate: 2017-07-18
  • Erratum to: Electrostatic forces drive poleward chromosome motions at

    • PubDate: 2017-07-03
  • Multiple molecular interactions redundantly contribute to RB-mediated cell
           cycle control

    • Abstract: Background The G1-S phase transition is critical to maintaining proliferative control and preventing carcinogenesis. The retinoblastoma tumor suppressor is a key regulator of this step in the cell cycle. Results Here we use a structure–function approach to evaluate the contributions of multiple protein interaction surfaces on pRB towards cell cycle regulation. SAOS2 cell cycle arrest assays showed that disruption of three separate binding surfaces were necessary to inhibit pRB-mediated cell cycle control. Surprisingly, mutation of some interaction surfaces had no effect on their own. Rather, they only contributed to cell cycle arrest in the absence of other pRB dependent arrest functions. Specifically, our data shows that pRB–E2F interactions are competitive with pRB–CDH1 interactions, implying that interchangeable growth arrest functions underlie pRB’s ability to block proliferation. Additionally, disruption of similar cell cycle control mechanisms in genetically modified mutant mice results in ectopic DNA synthesis in the liver. Conclusions Our work demonstrates that pRB utilizes a network of mechanisms to prevent cell cycle entry. This has important implications for the use of new CDK4/6 inhibitors that aim to activate this proliferative control network.
      PubDate: 2017-03-14
  • Systematic epistatic mapping of cellular processes

    • Abstract: Abstract Genetic screens have identified many novel components of various biological processes, such as components required for cell cycle and cell division. While forward genetic screens typically generate unstructured ‘hit’ lists, genetic interaction mapping approaches can identify functional relations in a systematic fashion. Here, we discuss a recent study by our group demonstrating a two-step approach to first screen for regulators of the mitotic cell cycle, and subsequently guide hypothesis generation by using genetic interaction analysis. The screen used a high-content microscopy assay and automated image analysis to capture defects during mitotic progression and cytokinesis. Genetic interaction networks derived from process-specific features generate a snapshot of functional gene relations in those processes, which follow a temporal order during the cell cycle. This complements a recently published approach, which inferred directional genetic interactions reconstructing hierarchical relationships between genes across different phases during mitotic progression. In conclusion, this strategy leverages unbiased, genome-wide, yet highly sensitive and process-focused functional screening in cells.
      PubDate: 2017-01-06
  • The Irr1/Scc3 protein implicated in chromosome segregation in
           Saccharomyces cerevisiae has a dual nuclear-cytoplasmic localization

    • Abstract: Background Correct chromosome segregation depends on the sister chromatid cohesion complex. The essential, evolutionarily conserved regulatory protein Irr1/Scc3, is responsible for the complex loading onto DNA and for its removal. We found that, unexpectedly, Irr1 is present not only in the nucleus but also in the cytoplasm. Results We show that Irr1 protein is enriched in the cytoplasm upon arrest of yeast cells in G1 phase following nitrogen starvation, diauxic shift or α-factor action, and also during normal cell cycle. Despite the presence of numerous Crm1-dependent export signals, the cytoplasmic pool of Irr1 is not derived through export from the nucleus but instead is simply retained in the cytoplasm. Cytoplasmic Irr1 interacts with the Imi1 protein implicated in glutathione homeostasis and mitochondrial integrity. Conclusions Besides regulation of the sister chromatid cohesion complex in the nucleus Irr1 appears to have an additional role in the cytoplasm, possibly through interaction with the cytoplasmic protein Imi1.
      PubDate: 2017-01-03
  • Electrostatic forces drive poleward chromosome motions at kinetochores

    • Abstract: Background Recent experiments regarding Ndc80/Hec1 in force generation at kinetochores for chromosome motions have prompted speculation about possible models for interactions between positively charged molecules at kinetochores and negative charge at and near the plus ends of microtubules. Discussion A clear picture of how kinetochores and centrosomes establish and maintain a dynamic coupling to microtubules for force generation during the complex motions of mitosis remains elusive. The current paradigm of molecular cell biology requires that specific molecules, or molecular geometries, for force generation be identified. However, it is possible to explain several different mitotic motions—including poleward force production at kinetochores—within a classical electrostatics approach in terms of experimentally known charge distributions, modeled as surface and volume bound charges interacting over nanometer distances. Conclusion We propose here that implicating Ndc80/Hec1 as a bound volume positive charge distribution in electrostatic generation of poleward force at kinetochores is most consistent with a wide range of experimental observations on mitotic motions, including polar production of poleward force and chromosome congression.
      PubDate: 2016-10-28
  • Erratum to: The loop-less tm Cdc34 E2 mutant defective polyubiquitination
           in vitro and in vivo supports yeast growth in a manner dependent on Ubp14
           and Cka2

    • PubDate: 2016-10-06
  • The CSL proteins, versatile transcription factors and context dependent
           corepressors of the notch signaling pathway

    • Abstract: Abstract The Notch signaling pathway is a reiteratively used cell to cell communication pathway that triggers pleiotropic effects. The correct regulation of the pathway permits the efficient regulation of genes involved in cell fate decision throughout development. This activity relies notably on the CSL proteins, (an acronym for CBF-1/RBPJ-κ in Homo sapiens/Mus musculus respectively, Suppressor of Hairless in Drosophila melanogaster, Lag-1 in Caenorhabditis elegans) which is the unique transcription factor and DNA binding protein involved in this pathway. The CSL proteins have the capacity to recruit activation or repression complexes according to the cellular context. The aim of this review is to describe the different co-repressor proteins that interact directly with CSL proteins to form repression complexes thereby regulating the Notch signaling pathway in animal cells to give insights into the paralogous evolution of these co-repressors in higher eumetazoans and their subsequent effects at developmental processes.
      PubDate: 2016-09-27
  • Interferon gamma-induced apoptosis of head and neck squamous cell
           carcinoma is connected to indoleamine-2,3-dioxygenase via mitochondrial
           and ER stress-associated pathways

    • Abstract: Background Tumor response to immunotherapy is the consequence of a concerted crosstalk between cytokines and effector cells. Interferon gamma (IFNγ) is one of the common cytokines coordinating tumor immune response and the associated biological consequences. Although the role of IFNγ in the modulation of tumor immunity has been widely documented, the mechanisms regulating IFNγ-induced cell death, during the course of immune therapy, is not described in detail. Results IFNγ triggered apoptosis of CLS-354 and RPMI 2650 cells, enhanced the protein expression and activation of indoleamine 2,3-dioxygenase (IDO), and suppressed the basal expression of heme oxygenase-1(HO-1). Interestingly, IFNγ induced the loss of mitochondrial membrane potential (Δψm) and increased accumulation of reactive oxygen species (ROS). The cytokine also induced the activation of Janus kinase (JAK)/Signal Transducer and Activator of Transcription (STAT)1, apoptosis signal-regulating kinase 1 (ASK1), p38, c-jun-N-terminal kinase (JNK) and NF-κB pathways and the transcription factors STAT1, interferon regulatory factor 1 (IRF1), AP-1, ATF-2, NF-κB and p53, and expression of Noxa protein. Furthermore, IFNγ was found to trigger endoplasmic reticulum (ER) stress as evidenced by the cleavage of caspase-4 and activation of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and inositol-requiring-1α (IRE1α) pathways. Using specific inhibitors, we identified a potential role for IDO as apoptotic mediator in the regulation of IFNγ-induced apoptosis of head and neck squamous cell carcinoma (HNSCC) cells via Noxa-mediated mitochondrial dysregulation and ER stress. Conclusion In addition to the elucidation of the role of IDO in the modulation of apoptosis, our study provides new insights into the molecular mechanisms of IFNγ-induced apoptosis of HNSCC cells during the course of immune therapy.
      PubDate: 2016-08-02
  • Rpl22 is required for IME1 mRNA translation and meiotic induction in S.

    • Abstract: Background The transition from mitotic cell division to meiotic development in S. cerevisiae requires induction of a transient transcription program that is initiated by Ime1-dependent destruction of the repressor Ume6. Although IME1 mRNA is observed in vegetative cultures, Ime1 protein is not suggesting the presence of a regulatory system restricting translation to meiotic cells. Results This study demonstrates that IME1 mRNA translation requires Rpl22A and Rpl22B, eukaryotic-specific ribosomal protein paralogs of the 60S large subunit. In the absence of Rpl22 function, IME1 mRNA synthesis is normal in cultures induced to enter meiosis. However, Ime1 protein production is reduced and the Ume6 repressor is not destroyed in rpl22 mutant cells preventing early meiotic gene induction resulting in a pre-meiosis I arrest. This role for Rpl22 is not a general consequence of mutating non-essential large ribosomal proteins as strains lacking Rpl29 or Rpl39 execute meiosis with nearly wild-type efficiencies. Several results indicate that Rpl22 functions by enhancing IME1 mRNA translation. First, the Ime1 protein synthesized in rpl22 mutant cells demonstrates the same turnover rate as in wild-type cultures. In addition, IME1 transcript is found in polysome fractions isolated from rpl22 mutant cells indicating that mRNA nuclear export and ribosome association occurs. Finally, deleting the unusually long 5′UTR restores Ime1 levels and early meiotic gene transcription in rpl22 mutants suggesting that Rpl22 enhances translation through this element. Polysome profiles revealed that under conditions of high translational output, Rpl22 maintains high free 60S subunit levels thus preventing halfmer formation, a translation species indicative of mRNAs bound by an unpaired 40S subunit. In addition to meiosis, Rpl22 is also required for invasive and pseudohyphal growth. Conclusions These findings indicate that Rpl22A and Rpl22B are required to selectively translate IME1 mRNA that is required for meiotic induction and subsequent gametogenesis. In addition, our results imply a more general role for Rpl22 in cell fate switches responding to environmental nitrogen signals.
      PubDate: 2016-07-29
  • Insights into APC/C: from cellular function to diseases and therapeutics

    • Abstract: Abstract Anaphase-promoting complex/cyclosome (APC/C) is a multifunctional ubiquitin-protein ligase that targets different substrates for ubiquitylation and therefore regulates a variety of cellular processes such as cell division, differentiation, genome stability, energy metabolism, cell death, autophagy as well as carcinogenesis. Activity of APC/C is principally governed by two WD-40 domain proteins, Cdc20 and Cdh1, in and beyond cell cycle. In the past decade, the results based on numerous biochemical, 3D structural, mouse genetic and small molecule inhibitor studies have largely attracted our attention into the emerging role of APC/C and its regulation in biological function, human diseases and potential therapeutics. This review will aim to summarize some recently reported insights into APC/C in regulating cellular function, connection of its dysfunction with human diseases and its implication of therapeutics.
      PubDate: 2016-07-13
  • Cullin-RING ligases in regulation of autophagy

    • Abstract: Abstract Cullin-RING ligases (CRLs), the largest E3 ubiquitin ligase family, promote ubiquitination and degradation of various cellular key regulators involved in a broad array of physiological and pathological processes, including cell cycle progression, signal transduction, transcription, cardiomyopathy, and tumorigenesis. Autophagy, an intracellular catabolic reaction that delivers cytoplasmic components to lysosomes for degradation, is crucial for cellular metabolism and homeostasis. The dysfunction of autophagy has been proved to associate with a variety of human diseases. Recent evidences revealed the emerging roles of CRLs in the regulation of autophagy. In this review, we will focus mainly on recent advances in our understandings of the regulation of autophagy by CRLs and the cross-talk between CRLs and autophagy, two degradation systems. We will also discuss the pathogenesis of human diseases associated with the dysregulation of CRLs and autophagy. Finally, we will discuss current efforts and future perspectives on basic and translational research on CRLs and autophagy.
      PubDate: 2016-06-10
  • The structure and regulation of Cullin 2 based E3 ubiquitin ligases and
           their biological functions

    • Abstract: Background Cullin-RING E3 ubiquitin ligase complexes play a central role in targeting cellular proteins for ubiquitination-dependent protein turnover through 26S proteasome. Cullin-2 is a member of the Cullin family, and it serves as a scaffold protein for Elongin B and C, Rbx1 and various substrate recognition receptors to form E3 ubiquitin ligases. Main body of the abstract First, the composition, structure and the regulation of Cullin-2 based E3 ubiquitin ligases were introduced. Then the targets, the biological functions of complexes that use VHL, Lrr-1, Fem1b, Prame, Zyg-11, BAF250, Rack1 as substrate targeting subunits were described, and their involvement in diseases was discussed. A small molecule inhibitor of Cullins as a potential anti-cancer drug was introduced. Furthermore, proteins with VHL box that might bind to Cullin-2 were described. Finally, how different viral proteins form E3 ubiquitin ligase complexes with Cullin-2 to counter host viral defense were explained. Conclusions Cullin-2 based E3 ubiquitin ligases, using many different substrate recognition receptors, recognize a number of substrates and regulate their protein stability. These complexes play critical roles in biological processes and diseases such as cancer, germline differentiation and viral defense. Through the better understanding of their biology, we can devise and develop new therapeutic strategies to treat cancers, inherited diseases and viral infections.
      PubDate: 2016-05-23
  • The T-box transcription factor TBX3 drives proliferation by direct
           repression of the p21 WAF1 cyclin-dependent kinase inhibitor

    • Abstract: Background TBX3, a member of the T-box family of transcription factors, is essential in development and has emerged as an important player in the oncogenic process. TBX3 is overexpressed in several cancers and has been shown to contribute directly to tumour formation, migration and invasion. However, little is known about the molecular basis for its role in development and oncogenesis because there is a paucity of information regarding its target genes. The cyclin-dependent kinase inhibitor p21WAF1 plays a pivotal role in a myriad of processes including cell cycle arrest, senescence and apoptosis and here we provide a detailed mechanism to show that it is a direct and biologically relevant target of TBX3. Results Using a combination of luciferase reporter gene assays and in vitro and in vivo binding assays we show that TBX3 directly represses the p21WAF1 promoter by binding a T-element close to its initiator. Furthermore, we show that the TBX3 DNA binding domain is required for the transcriptional repression of p21WAF1 and that pseudo-phosphorylation of a serine proline motif (S190) located within this domain may play an important role in regulating this ability. Importantly, we demonstrate using knockdown and overexpression experiments that p21WAF1 repression by TBX3 is biologically significant and required for TBX3-induced cell proliferation of chondrosarcoma cells. Conclusions Results from this study provide a detailed mechanism of how TBX3 transcriptionally represses p21WAF1 which adds to our understanding of how it may contribute to oncogenesis.
      PubDate: 2016-04-22
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