The nuclear receptor co-repressor (N-CoR) utilizes repression domains I and III for interaction and co-repression with ETO. (Q40514072)

21 September 2017

The nuclear receptor co-repressor (N-CoR) utilizes repression domains I and III for interaction and co-repression with ETO. (English)

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21 September 2017

Jörn Lausen

1

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21 September 2017

Seongeun Cho

series ordinal

2

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21 September 2017

Shaohua Liu

series ordinal

3

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21 September 2017

Milton H Werner

series ordinal

4

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21 September 2017

language of work or name

English

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publication date

17 September 2004

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Journal of Biological Chemistry

21 September 2017

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21 September 2017

279

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21 September 2017

47

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21 September 2017

49281-49288

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Signaling networks: the origins of cellular multitasking

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Histone acetylation in chromatin structure and transcription

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Histone acetylation and transcriptional regulatory mechanisms

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The transcriptional coactivators p300 and CBP are histone acetyltransferases

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Tetrahymena histone acetyltransferase A: a homolog to yeast Gcn5p linking histone acetylation to gene activation

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A p300/CBP-associated factor that competes with the adenoviral oncoprotein E1A

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Ligand-independent repression by the thyroid hormone receptor mediated by a nuclear receptor co-repressor

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Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR

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Mad-Max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3

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A transcriptional co-repressor that interacts with nuclear hormone receptors

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Histone deacetylases: transcriptional repression with SINers and NuRDs

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Conjunction dysfunction: CBP/p300 in human disease.

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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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ETO, a target of t(8;21) in acute leukemia, makes distinct contacts with multiple histone deacetylases and binds mSin3A through its oligomerization domain

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Aberrant recruitment of the nuclear receptor corepressor-histone deacetylase complex by the acute myeloid leukemia fusion partner ETO.

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The t(8;21) fusion protein, AML1 ETO, specifically represses the transcription of the p14(ARF) tumor suppressor in acute myeloid leukemia.

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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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The ETO protein disrupted in t(8;21)-associated acute myeloid leukemia is a corepressor for the promyelocytic leukemia zinc finger protein

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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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Oligomerization of ETO is obligatory for corepressor interaction

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Gene targeting reveals a crucial role for MTG8 in the gut.

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XETOR regulates the size of the proneural domain during primary neurogenesis in Xenopus laevis.

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Gfi-1 attaches to the nuclear matrix, associates with ETO (MTG8) and histone deacetylase proteins, and represses transcription using a TSA-sensitive mechanism

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Atrophin-1, the dentato-rubral and pallido-luysian atrophy gene product, interacts with ETO/MTG8 in the nuclear matrix and represses transcription

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AML1 and the AML1-ETO fusion protein in the pathogenesis of t(8;21) AML.

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Structure and expression of the human MTG8/ETO gene

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The AML1-MTG8 leukemic fusion protein forms a complex with a novel member of the MTG8(ETO/CDR) family, MTGR1

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MTG8 proto-oncoprotein interacts with the regulatory subunit of type II cyclic AMP-dependent protein kinase in lymphocytes

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Multiple regions of ETO cooperate in transcriptional repression

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A complex containing N-CoR, mSin3 and histone deacetylase mediates transcriptional repression

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m-Bop, a repressor protein essential for cardiogenesis, interacts with skNAC, a heart- and muscle-specific transcription factor

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ETO interacting proteins

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Role of the transcription factor AML-1 in acute leukemia and hematopoietic differentiation

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The MYND motif is required for repression of basal transcription from the multidrug resistance 1 promoter by the t(8;21) fusion protein

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The adenovirus E1A binding protein BS69 is a corepressor of transcription through recruitment of N-CoR

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The CREB constitutive activation domain interacts with TATA-binding protein-associated factor 110 (TAF110) through specific hydrophobic residues in one of the three subdomains required for both activation and TAF110 binding

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Oligomerization of RAR and AML1 transcription factors as a novel mechanism of oncogenic activation.

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Signal-specific co-activator domain requirements for Pit-1 activation

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The nuclear receptor corepressor N-CoR regulates differentiation: N-CoR directly interacts with MyoD.

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Small changes in expression affect predisposition to tumorigenesis

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21 January 2018

Identifiers

DOI

10.1074/JBC.M407239200

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21 September 2017

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