ArticleMolecular endocrinology (Baltimore, Md.)2015
Selective coregulator function and restriction of steroid receptor chromatin occupancy by Hic-5.
Article in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Transcriptional coactivation by EHMT2 restricts glucocorticoid-induced insulin resistance in a study with male mice.Nature communications · 2023Article
- Development of a Bioinformatics Framework for Identification and Validation of Genomic Biomarkers and Key Immunopathology Processes and Controllers in Infectious and Non-infectious Severe Inflammatory Response Syndrome.Frontiers in immunology · 2020Article
- An emerging link between LIM domain proteins and nuclear receptors.Cellular and molecular life sciences : CMLS · 2018Review
- Article
- Aberrant control of NF-κB in cancer permits transcriptional and phenotypic plasticity, to curtail dependence on host tissue: molecular mode.Cancer biology & medicine · 2017Article
- Glucocorticoid receptor binding to chromatin is selectively controlled by the coregulator Hic-5 and chromatin remodeling enzymes.The Journal of biological chemistry · 2017Article
- Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Steroid receptors (SRs) bind specific DNA regulatory sequences, thereby activating and repressing gene expression. We previously showed that transcriptional coregulator Hic-5 facilitates glucocorticoid regulation of some genes but blocks glucocorticoid regulation of others. Here, in a genome-wide analysis, Hic-5 depletion dramatically increased the global number of sites occupied by glucocorticoid receptor (GR) α (the major GR isoform), and many binding sites blocked by Hic-5 were associated with genes for which Hic-5 also blocked glucocorticoid-regulated expression. Hic-5 had similar effects on GRγ (a splice variant of GRα) and estrogen receptor α (ERα), facilitating hormonal regulation of some genes and blocking hormonal regulation of others. As with GRα, Hic-5 blocking of hormonal gene regulation mediated by GRγ and ERα was associated with blocking of GRγ and ERα occupancy at nearby sites. Hic-5 supported hormonal regulation of many more genes for GRα than for GRγ or ERα and thus exhibited selective coregulator functions for different SRs. In contrast, the number of Hic-5-blocked genes was similar for all 3 SRs. In addition to classic coregulator activity, Hic-5 influences the genomic occupancy of multiple SRs and thereby blocks some aspects of hormonal regulation. Thus, Hic-5, because of its tissue-specific expression, could contribute to tissue-specific genomic occupancy and gene regulation by SRs.
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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.