Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The insulin-like signaling (ILS) pathway regulates metabolism and is known to modulate adult life span in C. elegans. Altered stress responses and resistance to a wide range of stressors are also associated with changes in ILS and contribute to enhanced longevity. The transcription factors DAF-16 and HSF-1 are key effectors of the longevity phenotype. We demonstrate that increased intrinsic thermotolerance, due to lower ILS, is not dependent on stress-induced transcriptional responses but instead requires active protein translation. Translation profiling experiments reveal genes that are posttranscriptionally regulated in response to altered ILS during heat shock in a DAF-16-dependent manner. Furthermore, several novel proteins are specifically required for ILS effects on thermotolerance. We propose that lowered ILS results in metabolic and physiological changes. These DAF-16-induced changes precondition a translational response under acute stress to modulate survival.
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PMID:Insulin-like signaling determines survival during stress via posttranscriptional mechanisms in C. elegans. 2081 92

All organisms sense and respond to environmental and physiological stress by inducing cell stress responses that protect core biosynthetic processes such as DNA repair, protein folding, and clearance of damaged proteins. Of these, the heat shock response (HSR) protects the proteome against acute exposure to elevated temperatures, oxidants, and heavy metals, for example, and to the chronic expression of metastable, aggregation-prone proteins associated with aging and diseases of protein conformation. Induction of the HSR leads to the rapid and robust expression of molecular chaperones and other cell-protective pathways to protect nascent chain synthesis and folding, to prevent misfolding and aggregation, and to promote recovery from stress-induced damage. This review examines the properties of the stress-responsive transcription factor, HSF-1, in the regulation of the HSR, our current understanding of the stress-sensing mechanisms that recognize and distinguish between acute stress such as heat shock and chronic proteostasis imbalance as occurs in neurodegenerative diseases, and the cell nonautonomous control of the HSR by neuronal signaling in metazoans. This complex, systems-wide interdependence ensures cellular health span and organismal life span.
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PMID:The heat shock response: systems biology of proteotoxic stress in aging and disease. 2237 71