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Titolo:
Heat shock factor 1-mediated thermotolerance prevents cell death and results in G(2)/M cell cycle arrest
Autore:
Luft, JC; Benjamin, IJ; Mestril, R; Dix, DJ;
Indirizzi:
US EPA, Reprod Toxicol Div, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA US EPA Res Triangle Pk NC USA 27711 es Lab, Res Triangle Pk, NC 27711 USA Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX 75235 USA Univ Texas Dallas TX USA 75235 r, Dept Internal Med, Dallas, TX 75235 USA Loyola Univ, Med Ctr, Dept Physiol, Maywood, IL 61053 USA Loyola Univ Maywood IL USA 61053 Ctr, Dept Physiol, Maywood, IL 61053 USA
Titolo Testata:
CELL STRESS & CHAPERONES
fascicolo: 4, volume: 6, anno: 2001,
pagine: 326 - 336
SICI:
1355-8145(200110)6:4<326:HSF1TP>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
STRESS-INDUCED APOPTOSIS; PROTEIN HSP70; TRANSCRIPTION FACTOR-1; APAF-1 APOPTOSOME; NITRIC-OXIDE; HEAT-SHOCK-PROTEIN-70; OVEREXPRESSION; PROTECTION; ACTIVATION; PHOSPHORYLATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Dix, DJ US EPA, Reprod Toxicol Div, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA US EPA Res Triangle Pk NC USA 27711 Res Triangle Pk, NC 27711 USA
Citazione:
J.C. Luft et al., "Heat shock factor 1-mediated thermotolerance prevents cell death and results in G(2)/M cell cycle arrest", CELL STR CH, 6(4), 2001, pp. 326-336

Abstract

Mammalian cells respond to environmental stress by activating heat shock transcription factors (eg, Hsf1) that regulate increased synthesis of heat shock proteins (Hsps). Hsps prevent the disruption of normal cellular mitosis, meiosis, or differentiation by environmental stressors. To further characterize this stress response, transformed wildtype Hsf1(+/+), and mutant Hsf1(-/-) mouse embryonic fibroblasts (MEFs) were exposed to (1) lethal heat (45 degreesC, 60 minutes), (2) conditioning heat (43 degreesC, 30 minutes),or (3) conditioning followed by lethal heat. Western blot analysis demonstrated that only Hsf 1(+/+) MEFs expressed inducible Hsp70s and Hsp25 following conditioning or conditioning and lethal heat. Exposure of either Hsf1(+/+) or Hsf1(-/-) MEFs to lethal heat resulted in cell death. However, if conditioning heat was applied 6 hours before lethal heat, more than 85% of Hsf1(+/+) MEFs survived, and cells in G(2)/M transiently increased 3-fold. Incontrast, conditioned Hsf1(-/-) MEFs neither survived lethal heat nor exhibited this G(2)/M accumulation. Coinfection with adenoviral Hsp70 and Hsp25constructs did not fully recreate thermotolerance in either Hsf1 (-/-) or Hsf 1(-/-) MEFs, indicating other Hsf1-mediated gene expression is requiredfor complete thermotolerance. These results demonstrate the necessity of Hsf1-mediated gene expression for thermotolerance and the involvement of cell cycle regulation, particularly the G(2)/M transition, in this thermotolerant response.

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Documento generato il 29/03/20 alle ore 09:14:39