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Titolo:
Resveratrol-induced activation of p53 and apoptosis is mediated by extracellular-signal-regulated protein kinases and p38 kinase
Autore:
She, QB; Bode, AM; Ma, WY; Chen, NY; Dong, ZG;
Indirizzi:
Univ Minnesota, Hormel Inst, Austin, MN 55912 USA Univ Minnesota Austin MN USA 55912 ota, Hormel Inst, Austin, MN 55912 USA
Titolo Testata:
CANCER RESEARCH
fascicolo: 4, volume: 61, anno: 2001,
pagine: 1604 - 1610
SICI:
0008-5472(20010215)61:4<1604:RAOPAA>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
DAMAGE-INDUCED PHOSPHORYLATION; NECROSIS-FACTOR-ALPHA; N-TERMINAL KINASE; C-JUN KINASE; DNA-DAMAGE; AP-1 TRANSACTIVATION; JB6 CELLS; JNK ACTIVATION; IN-VITRO; HA-RAS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Dong, ZG Univ Minnesota, Hormel Inst, 801 16th Ave NE, Austin, MN 55912 USA Univ Minnesota 801 16th Ave NE Austin MN USA 55912 , MN 55912 USA
Citazione:
Q.B. She et al., "Resveratrol-induced activation of p53 and apoptosis is mediated by extracellular-signal-regulated protein kinases and p38 kinase", CANCER RES, 61(4), 2001, pp. 1604-1610

Abstract

Resveratrol, a phytoalexin found in grapes, berries, and peanuts, is one of the most promising agents for cancer prevention. Our previous study showed that the antitumor activity of resveratrol occurs through p53-mediated apoptosis. In this study, we have elucidated the potential signaling components underlying resveratrol-induced p53 activation and induction of apoptosis. We found that in a mouse JB6 epidermal cell line, resveratrol activated extacellular-signal-regulated protein kinases (ERKs), c-Jun NH2-terminal kinases (JNKs), and p38 kinase and induced serine 15 phosphorylation of p53. Stable expression of a dominant negative mutant of ERK2 or p38 kinase or their respective inhibitor, PD98059 or SB202190, repressed the phosphorylationof p53 at serine 15. In contrast, overexpression of a dominant negative mutant of JNK1 had no effect on the phosphorylation. Most importantly, ERKs and p38 kinase formed a complex with p53 after treatment with resveratrol. Strikingly, resveratrol-activated ERKs and p38 kinase, but not JNKs, phosphorylated p53 at serine 15 in vitro. Furthermore, pretreatment of the cells with PD98059 or SB202190 or stable expression of a dominant negative mutant of ERE;2 or p38 kinase impaired resveratrol-induced p53-dependent transcriptional activity and apoptosis, whereas constitutively active MEK1 increasedthe transcriptional activity of p53. These data strongly suggest that bothERKs and p38 kinase mediate resveratrol-induced activation of p53 and apoptosis through phosphorylation of p53 at serine 15.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 17:40:31