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Titolo:
A mechanism of repression by acute myeloid leukemia-1, the target of multiple chromosomal translocations in acute leukemia
Autore:
Lutterbach, B; Westendorf, JJ; Linggi, B; Isaac, S; Seto, E; Hiebert, SW;
Indirizzi:
Vanderbilt Univ, Sch Med, Vanderbilt Canc Ctr, Dept Biochem, Nashville, TN37232 USA Vanderbilt Univ Nashville TN USA 37232 pt Biochem, Nashville, TN37232 USA Vanderbilt Univ, Sch Med, Vanderbilt Canc Ctr, Dept Med, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Dept Med, Nashville, TN 37232 USA Bethel Coll, Dept Biol, N Newton, KS 67117 USA Bethel Coll N Newton KS USA 67117 Coll, Dept Biol, N Newton, KS 67117 USA Univ S Florida, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 anc Ctr & Res Inst, Tampa, FL 33612 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 1, volume: 275, anno: 2000,
pagine: 651 - 656
SICI:
0021-9258(20000107)275:1<651:AMORBA>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
DROSOPHILA SEGMENTATION GENE; ACUTE LYMPHOBLASTIC-LEUKEMIA; RUNT DOMAIN; AML1 GENE; OSTEOBLAST DIFFERENTIATION; TRANSCRIPTIONAL ACTIVATION; CLEIDOCRANIAL DYSPLASIA; FUNCTIONAL DOMAINS; C/EBP-ALPHA; N-COR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Hiebert, SW Vanderbilt Univ, Sch Med, Vanderbilt Canc Ctr, Dept Biochem, Med Res Bldg 2,Rm 512,23rd & Pierce, Nashville, TN 37232 USA Vanderbilt UnivMed Res Bldg 2,Rm 512,23rd & Pierce Nashville TN USA 37232
Citazione:
B. Lutterbach et al., "A mechanism of repression by acute myeloid leukemia-1, the target of multiple chromosomal translocations in acute leukemia", J BIOL CHEM, 275(1), 2000, pp. 651-656

Abstract

AML1 is one of the most frequently translocated genes in human leukemia. Here we demonstrate that acute myeloid leukemia-1 (AML-1) (Runx-1) repressestranscription from a native promoter, p21(Waf1/Cip1). Unexpectedly, this repression did not require interactions with the Groucho co-repressor. To define the mechanism of repression, we asked whether other co-repressors could interact with AML-1. We demonstrate that AML-1 interacts with the mSin3 co-repressors. Moreover, endogenous AML-1 associated with endogenous mSin3A in mammalian cells. A deletion mutant of AML-1 that did not interact with mSin3A failed to repress transcription. The AML-1/mSin3 association suggestsa mechanism of repression for the chromosomal translocation fusion proteins that disrupt AML-1.

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Documento generato il 30/03/20 alle ore 13:30:10