ArticleThe EMBO journal2000
Targeting of N-CoR and histone deacetylase 3 by the oncoprotein v-erbA yields a chromatin infrastructure-dependent transcriptional repression pathway.
Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 80 citations in OpenAlex.
- Functions and Mechanism of Thyroid Hormone Receptor Action During Amphibian Development.Endocrinology · 2024Review
- Unbiased screening identifies regulators of cell-cell adhesion and treatment options in pemphigus.Nature communications · 2024Article
- Chromatin-mediated regulation of cytomegalovirus gene expression.Virus research · 2011Review
- Oncogenic conversion of the thyroid hormone receptor by altered nuclear transport.Nuclear receptor signaling · 2006Article
- Article
- HdaA, a major class 2 histone deacetylase of Aspergillus nidulans, affects growth under conditions of oxidative stress.Eukaryotic cell · 2005Article
- Tumor suppressor SMAR1 mediates cyclin D1 repression by recruitment of the SIN3/histone deacetylase 1 complex.Molecular and cellular biology · 2005Article
- Histone deacetylase 3 (HDAC3) activity is regulated by interaction with protein serine/threonine phosphatase 4.Genes & development · 2005Article
- Activation of the growth-differentiation factor 11 gene by the histone deacetylase (HDAC) inhibitor trichostatin A and repression by HDAC3.Molecular and cellular biology · 2004Article
- The highly conserved region of the co-repressor Sin3A functionally interacts with the co-repressor Alien.Nucleic acids research · 2004Article
- Retinoic acid receptor alpha fusion to PML affects its transcriptional and chromatin-remodeling properties.Molecular and cellular biology · 2003Article
- The N-CoR/histone deacetylase 3 complex is required for repression by thyroid hormone receptor.Molecular and cellular biology · 2003Article
- Fragile X (CGG)n repeats induce a transcriptional repression in cis upon a linked promoter: evidence for a chromatin mediated effect.BMC molecular biology · 2003Article
- Nuclear receptor corepressor recruitment by unliganded thyroid hormone receptor in gene repression during Xenopus laevis development.Molecular and cellular biology · 2002Article
- JDP2, a repressor of AP-1, recruits a histone deacetylase 3 complex to inhibit the retinoic acid-induced differentiation of F9 cells.Molecular and cellular biology · 2002Article
- Chromatin disruption and histone acetylation in regulation of the human immunodeficiency virus type 1 long terminal repeat by thyroid hormone receptor.Molecular and cellular biology · 2002Article
- In vivo repression of an erythroid-specific gene by distinct corepressor complexes.The EMBO journal · 2002Article
- Histone deacetylase inhibitors induce remission in transgenic models of therapy-resistant acute promyelocytic leukemia.The Journal of clinical investigation · 2001Article
- The SMRT and N-CoR corepressors are activating cofactors for histone deacetylase 3.Molecular and cellular biology · 2001Article
- The histone deacetylase HDAC3 targets RbAp48 to the retinoblastoma protein.Nucleic acids research · 2001Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
Transcriptional repression by nuclear hormone receptors is thought to result from a unison of targeting chromatin modification and disabling the basal transcriptional machinery. We used Xenopus oocytes to compare silencing effected by the thyroid hormone receptor (TR) and its mutated version, the oncoprotein v-ErbA, on partly and fully chromatinized TR-responsive templates in vivo. Repression by v-ErbA was not as efficient as that mediated by TR, was significantly more sensitive to histone deacetylase (HDAC) inhibitor treatment and, unlike TR, v-ErbA required mature chromatin to effect repression. We find that both v-ErbA and TR can recruit the corepressor N-CoR, but, in contrast to existing models, show a concomitant enrichment for HDAC3 that occurs without an association with Sin3, HDAC1/RPD3, Mi-2 or HDAC5. We propose a requirement for chromatin infrastructure in N-CoR/HDAC3-effected repression and suggest that the inability of v-ErbA to silence on partly chromatinized templates may stem from its impaired capacity to interfere with basal transcriptional machinery function. In support of this notion, we find v-ErbA to be less competent than TR for binding to TFIIB in vitro and in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.