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Titolo:
Modulation of tolerance by mutant heat shock transcription factors
Autore:
Xia, WL; Vilaboa, N; Martin, JL; Mestril, R; Guo, YL; Voellmy, R;
Indirizzi:
Univ Miami, Sch Med, Dept Biochem & Mol Biol, Miami, FL 33136 USA Univ Miami Miami FL USA 33136 ept Biochem & Mol Biol, Miami, FL 33136 USA Univ Calif San Diego, Med Ctr, La Jolla, CA 92093 USA Univ Calif San Diego La Jolla CA USA 92093 ed Ctr, La Jolla, CA 92093 USA
Titolo Testata:
CELL STRESS & CHAPERONES
fascicolo: 1, volume: 4, anno: 1999,
pagine: 8 - 18
SICI:
1355-8145(199903)4:1<8:MOTBMH>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
DNA-BINDING ABILITY; PROTEIN DENATURATION; MAMMALIAN-CELLS; GENE-EXPRESSION; STRESS PROTEIN; HUMAN HSP70; RECOVERY; ACTIVATION; RESISTANCE; INDUCTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Voellmy, R UnivSAiami, Sch Med, Dept Biochem & Mol Biol, POB 016129, Miami, FL 33136 U Univ Miami POB 016129 Miami FL USA 33136 129, Miami, FL 33136 U
Citazione:
W.L. Xia et al., "Modulation of tolerance by mutant heat shock transcription factors", CELL STR CH, 4(1), 1999, pp. 8-18

Abstract

It ought to be possible to recruit normal cellular defenses to mitigate ischemia/reperfusion damage and to reduce toxicity of chemotherapeutic drugs. Stress-preconditioned cells acquire a tolerant state characterized by increased resistance to such insults. This state is widely believed to be mediated, partially, by heat shock proteins (Hsps). Indirect evidence suggests that stress-induced Hsp expression is controlled by heat shock transcriptionfactor 1 (Hsf1), which factor may therefore represent a preferred target for therapeutic modulation of tolerance. In support. positively acting (Hsf1(+)) and negatively acting (Hsf1(-)) mutants of Hsf1 were identified, inhibition of endogenous Hsf1 activity by Hsf1(-) prevents stress-induced Hsp synthesis and development of tolerance, Hsf1(+) drastically enhances expression of major Hsps in the absence of stress and induces tolerance against heat, simulated ischemia and toxicity by cyclophosphamide. Where compared, tolerance induced was slightly better than that produced by heat preconditioning. Thus, development of the tolerant state is dependent on increased levels of the cohort of Hsps induced by stress preconditioning, and Hsf1 can induce accumulation of a typical set of Hsps, which proteins are alone capableof providing tolerance at a similar level as heat preconditioning. These findings make Hsf1 a preferred target for pharmacological intervention to deliberately induce tolerance.

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Documento generato il 02/12/20 alle ore 08:09:52