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Titolo:
BAD/BCL-(xL) heterodimerization leads to bypass of G0/G1 arrest
Autore:
Chattopadhyay, A; Chiang, CW; Yang, E;
Indirizzi:
Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Dept Pediat, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 pt Pediat, Nashville, TN 37232 USA Vanderbilt Univ, Sch Med, Vanderbilt Ingram Canc Ctr, Dept Cell Biol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Cell Biol, Nashville, TN 37232 USA
Titolo Testata:
ONCOGENE
fascicolo: 33, volume: 20, anno: 2001,
pagine: 4507 - 4518
SICI:
0950-9232(20010727)20:33<4507:BHLTBO>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-CYCLE ENTRY; DEATH AGONIST BAD; BH3 DOMAIN; THYMOCYTE APOPTOSIS; BCL-2 EXPRESSION; TRANSGENIC MICE; PHOSPHORYLATION; SURVIVAL; PROTEIN; PROGRESSION;
Keywords:
BAD; BCL-(xL); apoptosis; cell cycle arrest;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Yang, E Vanderbilt Med Ctr, 525 MRB 2, Nashville, TN 37232 USA Vanderbilt Med Ctr 525 MRB 2 Nashville TN USA 37232 , TN 37232 USA
Citazione:
A. Chattopadhyay et al., "BAD/BCL-(xL) heterodimerization leads to bypass of G0/G1 arrest", ONCOGENE, 20(33), 2001, pp. 4507-4518

Abstract

The pro-apoptotic molecule BAD binds BCL-x(L) or BCL2 and inactivates their survival function. In addition to their anti-apoptotic function, BCL2 andBCL-xL also delay cell cycle entry from quiescence. We found that the BH3-only molecule BAD also exerted a cell cycle effect. BAD expression resultedin failure to cell cycle block in growth arrest conditions. In low serum and in confluence, fibroblasts constitutively or inducibly expressing BAD persisted in S phase, continued to incorporate BrdU, and exhibited sustained cyclin E/cdk2 activity. Mutation analysis indicated that the cell cycle effect of BAD was not dependent on its phosphorylation status or subcellular localization, but strictly co-segregated with BCL-xL binding. bclx(-/-) MEFsexpressing BAD and bad(-/-) MEFs both arrested in G0/G1 in low serum similar to wild-type controls, suggesting that the ability to overcome the G0/G1checkpoint resulted from the presence of BAD/BCL-x(L) heterodimers, ratherthan the absence of BCL-xL or BAD. These data provide evidence that in addition to regulating apoptosis, the BAD/BCLx(L) heterodimer has a novel cellcycle function.

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Documento generato il 29/09/20 alle ore 00:44:19