ArticleScientific reports2017
Genome-wide Regulatory Roles of the C2H2-type Zinc Finger Protein ZNF764 on the Glucocorticoid Receptor.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Glucocorticoids and Neutrophil Biology: Impact on the Development of Resistance to Glucocorticoid Therapy.Neuroimmunomodulation · 2026Review
- Levonorgestrel-induced modulation of triple negative breast cancer proliferation via glucocorticoid receptor.3 Biotech · 2025Article
- Role of circulating microRNAs in tetralogy of Fallot.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2025Article
- Prediction and assessment of deleterious and disease causing nonsynonymous single nucleotide polymorphisms (nsSNPs) in humanHeliyon · 2024Article
- Genome-Wide Identification of C2H2 ZFPs and Functional Analysis ofInternational journal of molecular sciences · 2022Article
- Tissue specific expression of sialic acid metabolic pathway: role in GNE myopathy.Journal of muscle research and cell motility · 2021Article
- SIRT1 is a transcriptional enhancer of the glucocorticoid receptor acting independently to its deacetylase activity.Molecular and cellular endocrinology · 2018Article
- C2H2-Type Zinc Finger Proteins: Evolutionarily Old and New Partners of the Nuclear Hormone Receptors.Nuclear receptor signaling · 2018Review
- CTCF As an Example of DNA-Binding Transcription Factors Containing Clusters of C2H2-Type Zinc Fingers.Acta naturaeArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The C2H2-type zinc finger protein ZNF764 acts as an enhancer for several steroid hormone receptors, and haploinsufficiency of this gene may be responsible for tissue resistance to multiple steroid hormones including glucocorticoids observed in a patient with 16p11.2 microdeletion. We examined genome-wide regulatory actions of ZNF764 on the glucocorticoid receptor (GR) in HeLa cells as a model system. ZNF764- and GR-binding sites demonstrated similar distribution in various genomic features. They positioned predominantly around 50-500 kbs from the transcription start sites of their nearby genes, and were closely localized with each other, overlapping in ~37% of them. ZNF764 demonstrated differential on/off effects on GR-binding and subsequent mRNA expression: some genes were highly dependent on the presence/absence of ZNF764, but others were not. Pathway analysis revealed that these 3 gene groups were involved in distinct cellular activities. ZNF764 physically interacted with GR at ligand-binding domain through its KRAB domain, and both its physical interaction to GR and zinc finger domain appear to be required for ZNF764 to regulate GR transcriptional activity. Thus, ZNF764 is a cofactor directing GR transcriptional activity toward specific biologic pathways by changing GR binding and transcriptional activity on the glucocorticoid-responsive genes.
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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.