ArticleThe Journal of biological chemistry2013
A conserved protein motif is required for full modulatory activity of negative elongation factor subunits NELF-A and NELF-B in modifying glucocorticoid receptor-regulated gene induction properties.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- DFF-ChIP: a method to detect and quantify complex interactions between RNA polymerase II, transcription factors, and chromatin.Nucleic acids research · 2024Article
- Dissecting transcriptional amplification by MYC.eLife · 2020Article
- Wolf-Hirschhorn Syndrome-Associated Genes Are Enriched in Motile Neural Crest Cells and Affect Craniofacial Development inFrontiers in physiology · 2019Article
- An Approach to Greater Specificity for Glucocorticoids.Frontiers in endocrinology · 2018Review
- Kinetically Defined Mechanisms and Positions of Action of Two New Modulators of Glucocorticoid Receptor-regulated Gene Induction.The Journal of biological chemistry · 2016Article
- Kinetically-defined component actions in gene repression.PLoS computational biology · 2015Article
- Research resource: modulators of glucocorticoid receptor activity identified by a new high-throughput screening assay.Molecular endocrinology (Baltimore, Md.) · 2014Article
- A kinase-independent activity of Cdk9 modulates glucocorticoid receptor-mediated gene induction.Biochemistry · 2014Article
- Glucocorticoid receptor repression mediated by BRCA1 inactivation in ovarian cancer.BMC cancer · 2014Article
- Theory of partial agonist activity of steroid hormones.AIMS molecular scienceArticle
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
NELF-B is a BRCA1-interacting protein and subunit (with NELF-A, -C/D, and -E) of the human negative elongation factor (NELF) complex, which participates in RNA polymerase II pausing shortly after transcription initiation, especially for synchronized gene expression. We now report new activities of NELF-B and other NELF complex subunits, which are to attenuate glucocorticoid receptor (GR)-mediated gene induction, reduce the partial agonist activity of an antagonist, and increase the EC50 of an agonist during nonsynchronized expression of exogenous and endogenous reporters. Stable knockdown of endogenous NELF-B has the opposite effects on an exogenous gene. The GR ligand-binding domain suffices for these biological responses. ChIP assays reveal that NELF-B diminishes GR recruitment to promoter regions of two endogenous genes. Using a new competition assay, NELF-A and NELF-B are each shown to act independently as competitive decelerators at two steps after the site of GR action and before or at the site of reporter gene activity. A common motif in each NELF was identified that is required for full activity of both NELF-A and NELF-B. These studies allow us to position the actions of two new modulators of GR-regulated transactivation, NELF-A and NELF-B, relative to other factors in the overall gene induction sequence.
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