The t(3;21) fusion product, AML1/Evi-1 blocks AML1-induced transactivation by recruiting CtBP.
about
C-Terminal Binding Protein: A Molecular Link between Metabolic Imbalance and Epigenetic Regulation in Breast Cancer.Role of AML1/Runx1 in the pathogenesis of hematological malignancies.Predicting the effect of transcription therapy in hematologic malignancies.The role of aberrant transcription factor in the progression of chronic myeloid leukemia.A role for RUNX1 in hematopoiesis and myeloid leukemia.Expression profiling reveals a distinct transcription signature in follicular thyroid carcinomas with a PAX8-PPAR(gamma) fusion oncogene.Histone deacetylase inhibitors trichostatin A and valproic acid circumvent apoptosis in human leukemic cells expressing the RUNX1 chimera.Fadd and Skp2 are possible downstream targets of RUNX1-EVI1.Association of polymorphism in the prolactin promoter and egg quality traits in laying hens.RUNX1/EVI1, which blocks myeloid differentiation, inhibits CCAAT-enhancer binding protein alpha function.
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P2860
The t(3;21) fusion product, AML1/Evi-1 blocks AML1-induced transactivation by recruiting CtBP.
description
2002 nî lūn-bûn
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2002年の論文
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2002年学术文章
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2002年学术文章
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2002年学术文章
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2002年学术文章
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name
The t(3;21) fusion product, AM ...... activation by recruiting CtBP.
@en
type
label
The t(3;21) fusion product, AM ...... activation by recruiting CtBP.
@en
prefLabel
The t(3;21) fusion product, AM ...... activation by recruiting CtBP.
@en
P2093
P2860
P356
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The t(3;21) fusion product, AM ...... sactivation by recruiting CtBP
@en
P2093
Hisamaru Hirai
Kazuhiro Maki
Kinuko Mitani
Mineo Kurokawa
Takashi Asai
Yoichi Imai
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P2888
P304
P356
10.1038/SJ.ONC.1205356
P407
P577
2002-04-01T00:00:00Z
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P6179
1053236787