ArticlePloS one2010
ZNF274 recruits the histone methyltransferase SETDB1 to the 3' ends of ZNF genes.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 179 citations in OpenAlex.
- AlphaGenome Atlas:medRxiv : the preprint server for health sciences · 2026Article
- LINE-1 Deregulation in Ovarian Cancer: Implications for Diagnosis, Prognosis, and Therapeutic Targeting.Molecular diagnosis & therapy · 2026Review
- ZNF274 constrains lineage plasticity and drives intrinsic resistance to CDK7 inhibitors in pancreatic cancer.Nature communications · 2026Article
- Extracellular condensates (ECs) are endogenous modulators of HIV transcription and latency reactivation.Molecular psychiatry · 2026Article
- The Many Faces of SetDB1.Epigenomes · 2026Review
- During the Formation of Vasculogenic Mimicry by Melanoma Cells, the Silencing of Two Sets of Developmental Genes Is Coupled Either with an Increase or a Decrease in Contacts with the Nucleoli.International journal of molecular sciences · 2025Article
- The Role of Histone Methyltransferase SETDB1 in Normal and Malignant Hematopoiesis.Cancer science · 2025Review
- Evolutionarily recent transcription factors partake in human cell cycle regulation.Cell genomics · 2025Article
- Histone H3 lysine methyltransferase activities control compartmentalization of human centromeres.bioRxiv : the preprint server for biology · 2025Article
- Regulation of epigenetics and chromosome structure by human ORC2.Cell reports · 2025Article
- SETDB1 activity is globally directed by H3K14 acetylation via its Triple Tudor Domain.Nucleic acids research · 2024Article
- Clusters of lineage-specific genes are anchored by ZNF274 in repressive perinucleolar compartments.Science advances · 2024Article
- Identifying microRNAs Possibly Implicated in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Fibromyalgia: A Review.International journal of molecular sciences · 2024Review
- SETDB1 deletion causes DNA demethylation and upregulation of multiple zinc-finger genes.Molecular biology reports · 2024Article
- Repression of developmental transcription factor networks triggers aging-associated gene expression in human glial progenitor cells.Nature communications · 2024Article
- Acetylcytidine modification of DDX41 and ZNF746 byFrontiers in oncology · 2024Article
- Article
- Z-flipon variants reveal the many roles of Z-DNA and Z-RNA in health and disease.Life science alliance · 2023Article
- Review
- Atlas of regulated target genes of transcription factors (ART-TF) in human ES cells.BMC bioinformatics · 2022Article
54 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Only a small percentage of human transcription factors (e.g. those associated with a specific differentiation program) are expressed in a given cell type. Thus, cell fate is mainly determined by cell type-specific silencing of transcription factors that drive different cellular lineages. Several histone modifications have been associated with gene silencing, including H3K27me3 and H3K9me3. We have previously shown that genes for the two largest classes of mammalian transcription factors are marked by distinct histone modifications; homeobox genes are marked by H3K27me3 and zinc finger genes are marked by H3K9me3. Several histone methyltransferases (e.g. G9a and SETDB1) may be involved in mediating the H3K9me3 silencing mark. We have used ChIP-chip and ChIP-seq to demonstrate that SETDB1, but not G9a, is associated with regions of the genome enriched for H3K9me3. One current model is that SETDB1 is recruited to specific genomic locations via interaction with the corepressor TRIM28 (KAP1), which is in turn recruited to the genome via interaction with zinc finger transcription factors that contain a Kruppel-associated box (KRAB) domain. However, specific KRAB-ZNFs that recruit TRIM28 (KAP1) and SETDB1 to the genome have not been identified. We now show that ZNF274 (a KRAB-ZNF that contains 5 C2H2 zinc finger domains), can interact with KAP1 both in vivo and in vitro and, using ChIP-seq, we show that ZNF274 binding sites co-localize with SETDB1, KAP1, and H3K9me3 at the 3' ends of zinc finger genes. Knockdown of ZNF274 with siRNAs reduced the levels of KAP1 and SETDB1 recruitment to the binding sites. These studies provide the first identification of a KRAB domain-containing ZNF that is involved in recruitment of the KAP1 and SETDB1 to specific regions of the human genome.
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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.