ArticleThe Journal of biological chemistry2016
Selective Recognition of H3.1K36 Dimethylation/H4K16 Acetylation Facilitates the Regulation of All-trans-retinoic Acid (ATRA)-responsive Genes by Putative Chromatin Reader ZMYND8.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- The chromatin reader ZMYND8 recruits the NuRD component GATAD2A through its MYND domain to regulate MAPT213 long noncoding RNA transcription.The Journal of biological chemistry · 2026Article
- Article
- The novel retinoid WYC-209 sensitizes multiple myeloma to carfilzomib via epigenetically upregulating ZMYND8.Experimental hematology & oncology · 2026Article
- Defining the heterogeneous molecular landscape of lung cancer cell responses to epigenetic inhibition.Communications biology · 2026Article
- Polarity protein Par3 deficiency promotes metastasis of bladder cancer via interaction of Ppp1r12c.Biology direct · 2026Article
- RACK7 senses and fine-tunes enhancer activity.iScience · 2025Article
- RhIL-11 reverses liver damage in septic mice by STAT3-mediated M-MDSCs induction modulated by a parallel mTORC1 signaling branch.Journal of inflammation (London, England) · 2025Article
- RACK7 Interacts with PRC2 Complex to Regulate Astrocyte Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ZMYND8 Reads H3K36me2 to Activate CEBPE Transcription and Suppress Multiple Myeloma Progression through the Inhibition of Adaptive UPR Pathways.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- GATAD2B is required for pre-implantation embryonic development by regulating zygotic genome activation.Cell proliferation · 2024Article
- Identification and validation of the nicotine metabolism-related signature of bladder cancer by bioinformatics and machine learning.Frontiers in immunology · 2024Article
- Zinc finger myeloid Nervy DEAF-1 type (ZMYND) domain containing proteins exert molecular interactions to implicate in carcinogenesis.Discover oncology · 2022Review
- ARID1A-dependent maintenance of H3.3 is required for repressive CHD4-ZMYND8 chromatin interactions at super-enhancers.BMC biology · 2022Article
- ZMYND8 suppresses MAPT213 LncRNA transcription to promote neuronal differentiation.Cell death & disease · 2022Article
- ZMYND8 is a master regulator of 27-hydroxycholesterol that promotes tumorigenicity of breast cancer stem cells.Science advances · 2022Article
- KDF1 Promoted Proliferation and Metastasis of Epithelial Ovarian CancerFrontiers in genetics · 2022Article
- Functional Roles of Bromodomain Proteins in Cancer.Cancers · 2021Review
- The Dual Function of KDM5C in Both Gene Transcriptional Activation and Repression Promotes Breast Cancer Cell Growth and Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- ZMYND8 preferentially binds phosphorylated EZH2 to promote a PRC2-dependent to -independent function switch in hypoxia-inducible factor-activated cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Regulation of ZMYND8 to Treat Cancer.Molecules (Basel, Switzerland) · 2021Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ZMYND8 (zinc finger MYND (Myeloid, Nervy and DEAF-1)-type containing 8), a newly identified component of the transcriptional coregulator network, was found to interact with the Nucleosome Remodeling and Deacetylase (NuRD) complex. Previous reports have shown that ZMYND8 is instrumental in recruiting the NuRD complex to damaged chromatin for repressing transcription and promoting double strand break repair by homologous recombination. However, the mode of transcription regulation by ZMYND8 has remained elusive. Here, we report that through its specific key residues present in its conserved chromatin-binding modules, ZMYND8 interacts with the selective epigenetic marks H3.1K36Me2/H4K16Ac. Furthermore, ZMYND8 shows a clear preference for canonical histone H3.1 over variant H3.3. Interestingly, ZMYND8 was found to be recruited to several developmental genes, including the all-trans-retinoic acid (ATRA)-responsive ones, through its modified histone-binding ability. Being itself inducible by ATRA, this zinc finger transcription factor is involved in modulating other ATRA-inducible genes. We found that ZMYND8 interacts with transcription initiation-competent RNA polymerase II phosphorylated at Ser-5 in a DNA template-dependent manner and can alter the global gene transcription. Overall, our study identifies that ZMYND8 has CHD4-independent functions in regulating gene expression through its modified histone-binding ability.
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