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  • 1
    Publication Date: 2014-10-18
    Description: The conserved heat shock transcription factor-1 (HSF-1) is essential to cellular stress resistance and life-span determination. The canonical function of HSF-1 is to regulate a network of genes encoding molecular chaperones that protect proteins from damage caused by extrinsic environmental stress or intrinsic age-related deterioration. In Caenorhabditis elegans, we engineered a modified HSF-1 strain that increased stress resistance and longevity without enhanced chaperone induction. This health assurance acted through the regulation of the calcium-binding protein PAT-10. Loss of pat-10 caused a collapse of the actin cytoskeleton, stress resistance, and life span. Furthermore, overexpression of pat-10 increased actin filament stability, thermotolerance, and longevity, indicating that in addition to chaperone regulation, HSF-1 has a prominent role in cytoskeletal integrity, ensuring cellular function during stress and aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403873/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4403873/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baird, Nathan A -- Douglas, Peter M -- Simic, Milos S -- Grant, Ana R -- Moresco, James J -- Wolff, Suzanne C -- Yates, John R 3rd -- Manning, Gerard -- Dillin, Andrew -- 1K99AG042495-01A1/AG/NIA NIH HHS/ -- 5P41RR011823-17/RR/NCRR NIH HHS/ -- 8 P41 GM103533-17/GM/NIGMS NIH HHS/ -- P01 AG031097/AG/NIA NIH HHS/ -- P40 OD010440/OD/NIH HHS/ -- P41 GM103533/GM/NIGMS NIH HHS/ -- R01AG027463-04/AG/NIA NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):360-3. doi: 10.1126/science.1253168.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California Berkeley, Berkeley, CA 94720, USA. ; Department of Computational Medicine and Bioinformatics, University of Michigan Medical School, Ann Arbor, MI 48109, USA. ; Scripps Research Institute, La Jolla, CA 92037, USA. ; Genentech, South San Francisco, CA 94080, USA. ; Howard Hughes Medical Institute, University of California Berkeley, Berkeley, CA 94720, USA. dillin@berkeley.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324391" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/*pharmacology/*physiology ; Cytoskeleton/*physiology/ultrastructure ; Heat-Shock Response/genetics/*physiology ; Hot Temperature ; *Longevity ; RNA Interference ; Transcription Factors/genetics/*physiology ; Troponin C/genetics/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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