ArticleThe Journal of biological chemistry2009
TIF1beta/KAP-1 is a coactivator of the orphan nuclear receptor NGFI-B/Nur77.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Chromatin opening ability of pioneer factor Pax7 depends on unique isoform and C-terminal domain.Nucleic acids research · 2023Article
- TRIM28-dependent SUMOylation protects the adult ovary from activation of the testicular pathway.Nature communications · 2022Article
- Pax7 pioneer factor action requires both paired and homeo DNA binding domains.Nucleic acids research · 2021Article
- Nuclear Receptors as Regulators of Pituitary Corticotroph Pro-Opiomelanocortin Transcription.Cells · 2020Review
- KAP1 targets actively transcribed genomic loci to exert pleomorphic effects on RNA polymerase II activity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
- Pituitary cell translation and secretory capacities are enhanced cell autonomously by the transcription factor Creb3l2.Nature communications · 2019Article
- ZFP30 promotes adipogenesis through the KAP1-mediated activation of a retrotransposon-derived Pparg2 enhancer.Nature communications · 2019Article
- Characteristics of Nur77 and its ligands as potential anticancer compounds (Review).Molecular medicine reports · 2018Review
- POMC: The Physiological Power of Hormone Processing.Physiological reviews · 2018Review
- Endogenous Purification of NR4A2 (Nurr1) Identified Poly(ADP-Ribose) Polymerase 1 as a Prime Coregulator in Human Adrenocortical H295R Cells.International journal of molecular sciences · 2018Article
- KAP1 Regulates Regulatory T Cell Function and Proliferation in Both Foxp3-Dependent and -Independent Manners.Cell reports · 2018Article
- Epigenetic activation during T helper 17 cell differentiation is mediated by Tripartite motif containing 28.Nature communications · 2018Article
- Loss-of-function mutations in theEndocrine-related cancer · 2017Article
- Regulation of cAMP Responsive Element Binding Protein 3-Like 1 (Creb3l1) Expression by Orphan Nuclear Receptor Nr4a1.Frontiers in molecular neuroscience · 2017Article
- miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro.BMC neurology · 2016Article
- KAP1 is overexpressed in hepatocellular carcinoma and its clinical significance.International journal of clinical oncology · 2016Article
- TRIM28 as an independent prognostic marker plays critical roles in glioma progression.Journal of neuro-oncology · 2016Article
- Targeting Nrf2 in healthy and malignant ovarian epithelial cells: Protection versus promotion.Molecular oncology · 2015Article
- A KAP1 phosphorylation switch controls MyoD function during skeletal muscle differentiation.Genes & development · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In efforts to define mechanisms of transcriptional activation by the orphan nuclear receptor NGFI-B (Nur77), we identified TIF1beta by mass spectrometry within a nuclear protein complex containing NGFI-B. TIF1beta, also known as KAP-1 (KRAB domain-associated protein) or KRIP-1, acts as a transcriptional corepressor for many transcription factors, in particular for the Krüppel-associated box domain-containing zinc finger transcription factors. TIF1beta is also an intrinsic component of two chromatin remodeling and histone deacetylase complexes, the N-CoR1 and nucleosome remodeling and deacetylation complexes. In contrast to these activities, we report that TIF1beta is a coactivator of NGFI-B and that it is as potent as the SRC coactivators in this context. Using pull-down assays and immunoprecipitation, we showed that TIF1beta interacts directly with NGFI-B and with other Nur family members. NGFI-B is an important mediator of hypothalamic corticotropin-releasing hormone (CRH) activation of proopiomelanocortin (POMC) transcription, and TIF1beta enhances transcription mediated through the NGFI-B target, the Nur response element (NurRE). The NurRE binds Nur factor dimers and is responsive to signaling pathways. In keeping with the role of NGFI-B as mediator of CRH signaling, we found that TIF1beta is recruited to the POMC promoter following CRH stimulation and that TIF1beta potentiates CRH and protein kinase A signaling through the NurRE; it acts synergistically with the SRC2 coactivator. However, the actions of TIF1beta and SRC2 were mapped to different NGFI-B AF-1 subdomains. Taken together, these results indicate that TIF1beta is an important coactivator of NGFI-B-dependent transcription.
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