Opposing Activities Protect Against Age-Onset Proteotoxicity

Proteotoxicity HSF1 Heat shock factor Proteostasis
DOI: 10.1126/science.1124646 Publication Date: 2006-08-11T00:44:58Z
ABSTRACT
Aberrant protein aggregation is a common feature of late-onset neurodegenerative diseases, including Alzheimer's disease, which associated with the misassembly Aβ 1-42 peptide. Aggregation-mediated toxicity was reduced in Caenorhabiditis elegans when aging slowed by decreased insulin/insulin growth factor–1–like signaling (IIS). The downstream transcription factors, heat shock factor 1, and DAF-16 regulate opposing disaggregation activities to promote cellular survival response constitutive toxic aggregation. Because IIS pathway central regulation longevity youthfulness worms, flies, mammals, these results suggest mechanistic link between process aggregation-mediated proteotoxicity.
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