The t(3;21) fusion product, AML1/Evi-1 blocks AML1-induced transactivation by recruiting CtBP. (Q40736865)

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9 December 2019

title

The t(3;21) fusion product, AML1/Evi-1 blocks AML1-induced transactivation by recruiting CtBP (English)

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9 December 2019

1

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9 December 2019

Motoshi Ichikawa

4

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9 December 2019

author name string

Mineo Kurokawa

2

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9 December 2019

Yoichi Imai

3

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9 December 2019

Takashi Asai

5

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9 December 2019

Kazuhiro Maki

6

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9 December 2019

Kinuko Mitani

7

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9 December 2019

Hisamaru Hirai

8

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9 December 2019

language of work or name

English

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publication date

1 April 2002

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9 December 2019

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9 December 2019

volume

21

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9 December 2019

issue

17

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9 December 2019

page(s)

2695-2703

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1205356

9 December 2019

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Net, a negative Ras-switchable TCF, contains a second inhibition domain, the CID, that mediates repression through interactions with CtBP and de-acetylation

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Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML) in mice: a model for human AML

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A dynamic role for HDAC7 in MEF2-mediated muscle differentiation.

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Both TEL and AML-1 contribute repression domains to the t(12;21) fusion protein

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M-CSF: haematopoietic growth factor or inflammatory cytokine?

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Fusion of the TEL gene on 12p13 to the AML1 gene on 21q22 in acute lymphoblastic leukemia

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Histone deacetylase activity is required for full transcriptional repression by mSin3A

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The transcription factor Evi-1.

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Acetylation of general transcription factors by histone acetyltransferases

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The corepressor CtBP interacts with Evi-1 to repress transforming growth factor beta signaling

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Transcriptional regulation of the MDR1 gene by histone acetyltransferase and deacetylase is mediated by NF-Y.

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A novel C-terminal binding protein (CTBP2) is closely related to CTBP1, an adenovirus E1A-binding protein, and maps to human chromosome 21q21.3

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Functional significance of histone deacetylase diversity

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Interaction and functional cooperation of the leukemia-associated factors AML1 and p300 in myeloid cell differentiation

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The oncoprotein Evi-1 represses TGF-beta signalling by inhibiting Smad3

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The evi-1 oncoprotein inhibits c-Jun N-terminal kinase and prevents stress-induced cell death

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Oncogenic transcription factors in the human acute leukemias

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ETO, a target of t(8;21) in acute leukemia, interacts with the N-CoR and mSin3 corepressors

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Histone deacetylase inhibitors: inducers of differentiation or apoptosis of transformed cells

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Histone deacetylases: a common molecular target for differentiation treatment of acute myeloid leukemias?

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Alternative splicing and genomic structure of the AML1 gene involved in acute myeloid leukemia

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t(8;21) breakpoints on chromosome 21 in acute myeloid leukemia are clustered within a limited region of a single gene, AML1

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Nuclear receptor repression mediated by a complex containing SMRT, mSin3A, and histone deacetylase

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Efficient selection for high-expression transfectants with a novel eukaryotic vector

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AML1, the target of multiple chromosomal translocations in human leukemia, is essential for normal fetal liver hematopoiesis

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Haploinsufficiency of CBFA2 causes familial thrombocytopenia with propensity to develop acute myelogenous leukaemia

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ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complex

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CCAAT enhancer-binding protein (C/EBP) and AML1 (CBF alpha2) synergistically activate the macrophage colony-stimulating factor receptor promoter

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Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia

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Identifiers

DOI

10.1038/SJ.ONC.1205356

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:11965542%20AND%20SRC:MED&resulttype=core&format=json

Dimensions Publication ID

9 December 2019

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