Ask about this productRelated genes to: ZMYND11 Blocking Peptide
- Gene:
- ZMYND11 NIH gene
- Name:
- zinc finger MYND-type containing 11
- Previous symbol:
- -
- Synonyms:
- BS69
- Chromosome:
- 10p15.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-20
- Date modifiied:
- 2016-04-25
Related products to: ZMYND11 Blocking Peptide
Related articles to: ZMYND11 Blocking Peptide
- - Source: PubMed
Publication date: 2026/06/23
Zheng RuiLiu Zi-QinShen YingWang Xin-Tai - Multiple genetic association studies linked variants at ARID5B with predisposition to B-cell-derived acute lymphoblastic leukemia (B-ALL) in children. Still, the molecular function of ARID5B remains largely uncharacterized. Here, we employ a combination of proteomics, genomics, and transcriptomics to describe the molecular mechanisms of ARID5B. We identify that ARID5B interacts with MIER1, C16ORF87, HDAC1, and HDAC2 forming a chromatin repressor complex. By CUT&RUN, we mapped ARID5B binding in active regions of the genome, tethering HDAC1 and HDAC2 to distal regulatory elements and promoters. Genes actively repressed by the ARID5B repressor complex are involved in B-cell proliferation and B-cell-specific signaling. Together, we describe how ARID5B assembles into a repressor complex and regulates B-cell-specific processes. Understanding its molecular mechanism will help elucidating how noncoding germline variants at ARID5B predispose to B-ALL. - Source: PubMed
Kutschat Ana PFrommelt FabianSantini Brianda LMüller SophieBatty PaulAwasthi AnimeshKarbon GerlindeSuperti-Furga GiulioSeruggia Davide - ZMYND11 is the sole known reader of H3.3K36me3. It has been characterized as a transcriptional repressor that fine-tunes RNA polymerase II (Pol II) elongation through recognition of gene body-localized H3K36me3, based primarily on earlier ChIP-seq data showing predominant ZMYND11 occupancy at gene bodies. However, subsequent data suggest that ZMYND11 may also localize to promoter regions. Here, using CUT&Tag assay, we demonstrate that ZMYND11 robustly occupies promoter regions in mouse ESCs and MEFs, with its promoter enrichment positively correlating with gene expression levels and Pol II occupancy. We further identify formaldehyde crosslinking as a critical factor causing signal loss at transcription start sites in conventional ChIP-seq. Mechanistically, ZMYND11 deficiency reduces the pausing index of Pol II, H3.3, and H3K36me3, indicating impaired transcription initiation. ZMYND11 knockout in mouse ESCs induces transcriptomic changes, impairs cell proliferation, and aberrantly activates 2-cell-specific transcriptional programs via ROS accumulation. Our findings reveal a previously unappreciated role for ZMYND11 as a transcriptional initiator that stabilizes Pol II at promoters, establishing its essential function in maintaining embryonic stem cell homeostasis and advancing our understanding of its context-dependent transcriptional regulatory mechanisms. - Source: PubMed
Tian YuWang Yu-FanCai XueJiang Xiao-HuaZhou Li-QuanYin Ying - The complex pathogenetic mechanisms of rare genetic diseases make the diagnostic process highly challenging. Advances in molecular genomic techniques, such as exome sequencing, have improved the identification of copy number variants (CNVs), increasing diagnostic yield. - Source: PubMed
Minale Elia Marco PaoloMartone StefaniaCriscuolo ChiaraMarra RobertaLasorsa Vito AlessandroRuggiero RaffaellaSuero TeresaCapasso MarioAndolfo ImmacolataIolascon AchilleRusso RobertaPinelli Michele - The crosstalk between tumor cells and stromal components in the tumor microenvironment critically influences colorectal cancer (CRC) progression and metastasis. The role of tumor-associated endothelial cells (TAECs) in this process is not fully understood. This study aimed to elucidate the function of miR-19b-3p in mediating CRC-endothelial cell communication. - Source: PubMed
Publication date: 2026/03/02
Cao YixinZhang JiaKai XinyuXue YongwangWang XuequanWang XiangyangZhang CaiHua ZhongyiWei YuanYin Runting