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Titolo:
Bcl-2 is an apoptotic target suppressed by both c-Myc and E2F-1
Autore:
Eischen, CM; Packham, G; Nip, J; Fee, BE; Hiebert, SW; Zambetti, GP; Cleveland, JL;
Indirizzi:
St Jude Childrens Hosp, Dept Biochem, Memphis, TN 38105 USA St Jude Childrens Hosp Memphis TN USA 38105 iochem, Memphis, TN 38105 USA Southampton Gen Hosp, CRC, Wessex Med Oncol Unit, Southampton SO16 6YD, Hants, England Southampton Gen Hosp Southampton Hants England SO16 6YD D, Hants, England Unilever Res US, Edgewater, NJ 07020 USA Unilever Res US Edgewater NJ USA07020 er Res US, Edgewater, NJ 07020 USA Vanderbilt Univ, Dept Biochem, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 t Biochem, Nashville, TN 37232 USA Univ Tennessee, Dept Biochem, Memphis, TN 38163 USA Univ Tennessee Memphis TN USA 38163 , Dept Biochem, Memphis, TN 38163 USA
Titolo Testata:
ONCOGENE
fascicolo: 48, volume: 20, anno: 2001,
pagine: 6983 - 6993
SICI:
0950-9232(20011025)20:48<6983:BIAATS>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-CYCLE ARREST; S-PHASE ENTRY; WILD-TYPE P53; MEDIATED APOPTOSIS; ORNITHINE DECARBOXYLASE; P53-DEPENDENT APOPTOSIS; HEMATOPOIETIC-CELLS; SEPARABLE FUNCTIONS; TRANSGENIC MICE; RAT FIBROBLASTS;
Keywords:
c-Myc; E2F-1; Bcl-2; Bcl-X-L; myeloid; apoptosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
76
Recensione:
Indirizzi per estratti:
Indirizzo: Cleveland, JL St Jude Childrens Hosp, Dept Biochem, 332 N Lauderdale St, Memphis, TN 38105 USA St Jude Childrens Hosp 332 N Lauderdale St Memphis TN USA 38105
Citazione:
C.M. Eischen et al., "Bcl-2 is an apoptotic target suppressed by both c-Myc and E2F-1", ONCOGENE, 20(48), 2001, pp. 6983-6993

Abstract

Malignant transformation occurs in cells that overexpress c-Myc or that inappropriately activate E2F-1. Transformation occurs after the selection of cells that have acquired resistance to apoptosis that is triggered by theseoncogenes, and a key mediator of this cell death process is the p53 tumor suppressor. In IL-3-dependent immortal 32D.3 myeloid cells the ARF/p53 apoptotic pathway is inactivated, as these cells fail to express ARF. Nonetheless, both c-Myc and E2F-1 overexpression accelerated apoptosis when these cells were deprived of IL-3. Here we report that c-Myc or E2F-1 overexpression suppresses Bcl-2 protein and RNA levels, and that restoration of Bcl-2 protein effectively blocks the accelerated apoptosis that occurs when c-Myc- or E2F-1-overexpressing cells are deprived of IL-3. Blocking p53 activity with mutant p53 did not abrogate E2F-1-induced suppression of Bcl-2. Analysis of immortal myeloid cells engineered to overexpress c-Myc and E2F-1 DNA binding mutants revealed that DNA binding activity of these oncoproteins is required to suppress Bcl-2 expression. These results suggest that the targeting of Bcl-2 family members is an important mechanism of oncogene-induced apoptosis, and that this occurs independent of the ARF/p53 pathway.

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Documento generato il 31/10/20 alle ore 00:15:40