共查询到20条相似文献,搜索用时 31 毫秒
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ETO, a target of t(8;21) in acute leukemia, makes distinct contacts with multiple histone deacetylases and binds mSin3A through its oligomerization domain 总被引:14,自引:0,他引:14 下载免费PDF全文
Amann JM Nip J Strom DK Lutterbach B Harada H Lenny N Downing JR Meyers S Hiebert SW 《Molecular and cellular biology》2001,21(19):6470-6483
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The ETO protein disrupted in t(8;21)-associated acute myeloid leukemia is a corepressor for the promyelocytic leukemia zinc finger protein 总被引:11,自引:0,他引:11 下载免费PDF全文
Melnick AM Westendorf JJ Polinger A Carlile GW Arai S Ball HJ Lutterbach B Hiebert SW Licht JD 《Molecular and cellular biology》2000,20(6):2075-2086
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ETO, a Target of t(8;21) in Acute Leukemia, Interacts with the N-CoR and mSin3 Corepressors 总被引:29,自引:7,他引:22 下载免费PDF全文
Bart Lutterbach Jennifer J. Westendorf Bryan Linggi Andrea Patten Mariko Moniwa James R. Davie Khanh D. Huynh Vivian J. Bardwell Robert M. Lavinsky Michael G. Rosenfeld Christopher Glass Edward Seto Scott W. Hiebert 《Molecular and cellular biology》1998,18(12):7176-7184
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Salat D Liefke R Wiedenmann J Borggrefe T Oswald F 《Molecular and cellular biology》2008,28(10):3502-3512
Notch is a transmembrane receptor that determines cell fates and pattern formation in all animal species. After specific ligand binding, the intracellular part of Notch is cleaved off and translocates to the nucleus, where it targets the DNA binding protein RBP-Jkappa. In the absence of Notch, RBP-Jkappa represses Notch target genes by recruiting a corepressor complex. We and others have previously identified SHARP as one component of this complex. Here, we show that the corepressor ETO as well as the leukemogenic fusion protein AML1/ETO directly interacts with SHARP, that ETO is part of the endogenous RBP-Jkappa-containing corepressor complex, and that ETO is found at Notch target gene promoters. In functional assays, corepressor ETO, but not AML1/ETO, augments SHARP-mediated repression in an histone deacetylase-dependent manner. Furthermore, either the knockdown of ETO or the overexpression of AML1/ETO activates Notch target genes. Therefore, we propose that AML1/ETO can disturb the normal, repressive function of ETO at Notch target genes. This activating (or derepressing) effect of AML1/ETO may contribute to its oncogenic potential in myeloid leukemia. 相似文献
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Iso T Sartorelli V Poizat C Iezzi S Wu HY Chung G Kedes L Hamamori Y 《Molecular and cellular biology》2001,21(17):6080-6089