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Titolo:
ETO, A TARGET OF T(8-21) IN ACUTE-LEUKEMIA, INTERACTS WITH THE N-COR AND MSIN3 COREPRESSORS
Autore:
LUTTERBACH B; WESTENDORF JJ; LINGGI B; PATTEN A; MONIWA M; DAVIE JR; HUYNH KD; BARDWELL VJ; LAVINSKY RM; ROSENFELD MG; GLASS C; SETO E; HIEBERT SW;
Indirizzi:
VANDERBILT UNIV,SCH MED,VANDERBILT CANC CTR,DEPT BIOCHEM,MED RES BLDGII,RM 512,23RD & PIERCE NASHVILLE TN 37232 VANDERBILT UNIV,SCH MED,VANDERBILT CANC CTR,DEPT BIOCHEM NASHVILLE TN37232 UNIV MANITOBA,DEPT BIOCHEM & MOL BIOL WINNIPEG MB R3E 0W3 CANADA UNIV MINNESOTA,BIOCHEM MOL BIOL & BIOPHYS GRAD PROGRAM MINNEAPOLIS MN55455 UNIV MINNESOTA,INST HUMAN GENET,DEPT BIOCHEM MINNEAPOLIS MN 55455 UNIV MINNESOTA,CTR CANC MINNEAPOLIS MN 55455 UNIV CALIF SAN DIEGO,SCH MED,DEPT MED LA JOLLA CA 92093 UNIV CALIF SAN DIEGO,SCH MED,HOWARD HUGHES MED INST LA JOLLA CA 92093 UNIV S FLORIDA,H LEE MOFFITT CANC CTR & RES INST TAMPA FL 33612
Titolo Testata:
Molecular and cellular biology (Print)
fascicolo: 12, volume: 18, anno: 1998,
pagine: 7176 - 7184
SICI:
0270-7306(1998)18:12<7176:EATOTI>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSCRIPTIONAL REPRESSION; HISTONE DEACETYLASE; FUSION TRANSCRIPT; INDEPENDENT REPRESSION; PROTEIN; RUNT; IDENTIFICATION; AML1/ETO; PROMOTER; COMPLEX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
47
Recensione:
Indirizzi per estratti:
Citazione:
B. Lutterbach et al., "ETO, A TARGET OF T(8-21) IN ACUTE-LEUKEMIA, INTERACTS WITH THE N-COR AND MSIN3 COREPRESSORS", Molecular and cellular biology (Print), 18(12), 1998, pp. 7176-7184

Abstract

t(8;21) is one of the most frequent translocations associated with acute myeloid leukemia. It produces a chimeric protein, acute myeloid leukemia-1 (AML-1)-eight-twenty-one (ETO), that contains the amino-terminal DNA binding domain of the AML-1 transcriptional regulator fused tonearly all of ETO. Here we demonstrate that ETO interacts with the nuclear receptor corepressor N-CoR, the mSin3 corepressors, and histone deacetylases. Endogenous ETO also cosediments on sucrose gradients with mSin3A, N-CoR, and histone deacetylases, suggesting that it is a component of one or more corepressor complexes. Deletion mutagenesis indicates that ETO interacts with mSin3A independently of its association with N-CoR, Single amino acid mutations that impair the ability of ETOto interact with the central portion of N-CoR affect the ability of the t(8;21) fusion protein to repress transcription. Finally, AML-1/ETOassociates with histone deacetylase activity and a histone deacetylase inhibitor impairs the ability of the fusion protein to repress transcription. Thus, t(8;21) fuses a component of a corepressor complex to AML-1 to repress transcription.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 08:02:09