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| http://dx.doi.org/10.3389/fmolb.2021.791009 | DOI Listing |
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Male sex determination maintains proteostasis and extends lifespan of daf-18/PTEN deficient C. elegans.
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The Zhongzhou Laboratory for Integrative Biology, Henan University, 450000, Zhengzhou, Henan, China.
Although females typically have a survival advantage, those with PTEN functional abnormalities face a higher risk of developing tumors than males. However, the differences in how each sex responds to PTEN dysfunction have rarely been studied. We use Caenorhabditis elegans to investigate how male and hermaphrodite worms respond to dysfunction of the PTEN homolog daf-18.
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J Clin Invest
January 2025
Department of Biomedical Engineering, Columbia University, New York, New York, USA.
Loss of Bcl2-associated athanogene 3 (BAG3) is associated with dilated cardiomyopathy (DCM). BAG3 regulates sarcomere protein turnover in cardiomyocytes; however, the function of BAG3 in other cardiac cell types is understudied. In this study, we used an isogenic pair of BAG3-knockout and wild-type human induced pluripotent stem cells (hiPSCs) to interrogate the role of BAG3 in hiPSC-derived cardiac fibroblasts (CFs).
View Article and Find Full Text PDFLocation of polyglutamine track affects pathogenic threshold of polyglutamine expansion diseases - Importance of association with the proteasome.
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January 2025
Laboratory of Molecular Neurodegeneration, Peter the Great St Petersburg State Polytechnical University, St Petersburg, 195251, Russian Federation. Electronic address:
The expansion of glutamine residue track (polyQ) within soluble proteins (Q proteins) is responsible for nine autosomal-dominant genetic neurodegenerative disorders. These disorders develop when polyQ expansion exceeds a specific pathogenic threshold (Q) which is unique for each disease. However, the pathogenic mechanisms associated with the variability of Q within the family of Q proteins are poorly understood.
View Article and Find Full Text PDFLarge-scale experimental analyses find ever more abundant evidence of translation from start codons upstream of the canonical start site. This translation either generates entirely new proteins (from novel upstream open reading frames) or produces isoforms with extended N-terminals when the novel start codon is in frame Most extended N-terminals are likely to just add a disordered region to the canonical protein isoform, but some may also block the recognition of the signal peptide causing the isoform to accumulate in the incorrect cellular compartment. This analysis finds evidence that upstream translations that would interfere with signal peptides are detected in expected quantities in ribosome profiling experiments, but that the equivalent N-terminally extended protein isoforms are significantly reduced in multiple proteomics experiments.
View Article and Find Full Text PDFUBA1 inhibition sensitizes cancer cells to PARP inhibitors.
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December 2024
Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Quantitative and Computational Biosciences Program, Baylor College of Medicine, Houston, TX, USA.
Therapeutic strategies targeting the DNA damage response, such as poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi), have revolutionized cancer treatment in tumors deficient in homologous recombination (HR). However, overcoming innate and acquired resistance to PARPi remains a significant challenge. Here, we employ a genome-wide CRISPR knockout screen and discover that the depletion of ubiquitin-activating enzyme E1 (UBA1) enhances sensitivity to PARPi in HR-proficient ovarian cancer cells.
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