ArticleMolecular endocrinology (Baltimore, Md.)2009
Crucial roles for interactions between MLL3/4 and INI1 in nuclear receptor transactivation.
Article in Molecular endocrinology (Baltimore, Md.), 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 49 citations in OpenAlex.
- Under-Representation of Racial Groups in Genomics Studies of Gastroenteropancreatic Neuroendocrine Neoplasms.Cancer research communications · 2022Article
- Reprogramming of the epigenome in neurodevelopmental disorders.Critical reviews in biochemistry and molecular biology · 2022Review
- Epigenetic disorders: Lessons from the animals-animal models in chromatinopathies.Frontiers in cell and developmental biology · 2022Review
- Review
- SET1/MLL family of proteins: functions beyond histone methylation.Epigenetics · 2021Review
- Interplay of BAF and MLL4 promotes cell type-specific enhancer activation.Nature communications · 2021Article
- The MLL/SET family and haematopoiesis.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020Review
- Why are so many MLL lysine methyltransferases required for normal mammalian development?Cellular and molecular life sciences : CMLS · 2019Review
- KMT2C mediates the estrogen dependence of breast cancer through regulation of ERα enhancer function.Oncogene · 2018Article
- Functional convergence of histone methyltransferases EHMT1 and KMT2C involved in intellectual disability and autism spectrum disorder.PLoS genetics · 2017Article
- Effect of agomelatine on memory deficits and hippocampal gene expression induced by chronic social defeat stress in mice.Scientific reports · 2017Article
- Transcriptional control of non-apoptotic developmental cell death in C. elegans.Cell death and differentiation · 2016Article
- Article
- Article
- Integrated genomic analysis suggests MLL3 is a novel candidate susceptibility gene for familial nasopharyngeal carcinoma.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2015Article
- Bisphenol-A induces expression of HOXC6, an estrogen-regulated homeobox-containing gene associated with breast cancer.Biochimica et biophysica acta · 2015Article
- Gene expression in superior temporal cortex of schizophrenia patients.European archives of psychiatry and clinical neuroscience · 2014Article
- Establishment of active chromatin structure at enhancer elements by mixed-lineage leukemia 1 to initiate estrogen-dependent gene expression.Nucleic acids research · 2014Article
- The role of maintenance proteins in the preservation of epithelial cell identity during mammary gland remodeling and breast cancer initiation.Chinese journal of cancer · 2014Review
- SET for life: biochemical activities and biological functions of SET domain-containing proteins.Trends in biochemical sciences · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Nuclear receptor (NR) transactivation involves multiple coactivators, and the molecular basis for how these are functionally integrated needs to be determined to fully understand the NR action. Activating signal cointegrator-2 (ASC-2), a transcriptional coactivator of many NRs and transcription factors, forms a steady-state complex, ASCOM (for ASC-2 complex), which contains histone H3-lysine-4 (H3K4) methyltransferase MLL3 or its paralog MLL4. Here, we show that ASCOM requires a functional cross talk with the ATPase-dependent chromatin remodeling complex Swi/Snf for efficient NR transactivation. Our results reveal that ASCOM and Swi/Snf are tightly colocalized in the nucleus and that ASCOM and Swi/Snf promote each other's binding to NR target genes. We further show that the C-terminal SET domain of MLL3 and MLL4 directly interacts with INI1, an integral subunit of Swi/Snf. Our mutational analysis demonstrates that this interaction underlies the mutual facilitation of ASCOM and Swi/Snf recruitment to NR target genes. Importantly, this study uncovers a specific protein-protein interaction as a novel venue to couple two distinct enzymatic coactivator complexes during NR transactivation.
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Registered trials
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.