MLL4 antibody - N-terminal region (ARP33704_T100)
- Known as:
- MLL4 (anti-) - N-terminal region (ARP33704_T100)
- Catalog number:
- arp33704_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MLL4 antibody - N-terminal region (ARP33704_T100)
Related genes to: MLL4 antibody - N-terminal region (ARP33704_T100)
- Gene:
- KMT2B NIH gene
- Name:
- lysine methyltransferase 2B
- Previous symbol:
- -
- Synonyms:
- KIAA0304, MLL2, TRX2, HRX2, WBP7, MLL1B, MLL4, CXXC10
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2013-05-09
- Date modifiied:
- 2018-03-06
- Gene:
- KMT2D NIH gene
- Name:
- lysine methyltransferase 2D
- Previous symbol:
- TNRC21, MLL2
- Synonyms:
- ALR, MLL4, CAGL114
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-14
- Date modifiied:
- 2018-03-06
Related products to: MLL4 antibody - N-terminal region (ARP33704_T100)
Related articles to: MLL4 antibody - N-terminal region (ARP33704_T100)
- Following implantation, the epiblast undergoes gastrulation to form the three germ layers, a process requiring precise temporal control of developmental gene expression. However, the mechanisms governing RNA polymerase II (Pol II) engagement at developmental gene promoters during this critical stage remain poorly understood. Here, we present a genome-wide analysis of Pol II occupancy in mouse post-implantation embryos, revealing that nearly half of bivalent promoters are bound by Pol II in a lineage-specific and temporally ordered manner. This recruitment follows a stepwise chromatin remodeling cascade, with initial deposition of H3K27me3, followed by H3K4me3 acquisition and Pol II engagement. Through genetic perturbation, we show that KMT2B promotes Pol II loading via H3K4me3 deposition, whereas the Polycomb component EED restricts this process by maintaining H3K27me3. Notably, we identify the transcription factor SP1 as a critical facilitator of Pol II recruitment at bivalent loci. SP1 binding coincides with reduced H3K27me3 levels and enhanced Pol II occupancy, and its loss leads to chromatin re-silencing and transcriptional failure. Together, our findings establish a chromatin-based regulatory framework in which SP1 and histone modifications cooperatively license the transcriptional activation of developmental genes during germ layer formation. - Source: PubMed
Shen XipengWen YutingTang XiaohanLiu YujiaoLi WensiChen WenhaoYang ShuhengWang LidanYang HaiboLiu KunyanLi LeiXiang Yunlong - Colorectal cancer remains a leading cause of cancer mortality in the United States and can be characterized by racial and sex-based disparities. The objective of the current study was to characterize the genomic heterogeneity of colorectal cancer among diverse demographic groups, assess coalteration patterns and their impact on long-term outcomes among patients with colorectal cancer. - Source: PubMed
Publication date: 2025/06/14
Stecko HunterTsilimigras Diamantis IIyer SidharthDaw JadZhu HuaHuang EmilyKalady MatthewPawlik Timothy M - Gastric adenocarcinoma is a highly lethal neoplasm with a short survival especially when metastatic. Few effective treatments are available for the control of the disease and palliation of patients with metastatic gastric cancer. Although progress has been made in the elucidation of molecular pathways invoked in gastric carcinogenesis, this knowledge has not yet led to major breakthroughs, in contrast to several other types of cancer. The role of stem cell transcription factors SOX2 and CDX2 is of particular interest in the pathogenesis of gastric cancer. - Source: PubMed
Publication date: 2025/02/26
Voutsadakis Ioannis A - Human endogenous retroviruses (HERVs) are inherited genetic elements derived from exogenous retroviral infections occurring throughout evolution. Accumulating evidence implicates increased expression of HERV type W envelope (HERV-W ENV) in psychiatric and neurodevelopmental disorders. To gain more mechanistic insights into the neurobiological disease pathways affected by HERV-W ENV expression, we took advantage of a mouse model that recapitulates the expression of the human-specific HERV-W ENV protein. Behavioral and cognitive phenotyping of transgenic (TG) mice expressing HERV-W ENV and wild-type (WT) controls showed that expression of this retroviral envelope caused deficits in numerous functional domains, including repetitive behavior, social and object recognition memory, and sensorimotor gating. Genome-wide RNA sequencing of hippocampal tissue demonstrated that transgenic expression of HERV-W ENV led to transcriptomic alterations that are highly relevant for psychiatric and neurodevelopmental disorders, cognitive functions, and synaptic development. Differential gene expression in TG mice encompassed a downregulation of several genes associated with schizophrenia and autism spectrum disorder, including Setd1a, Cacna1g, Ank3, and Shank3, as well as a downregulation of histone methyltransferase genes that belong to the Set1-like histone H3 lysine 4 (H3K4) methyltransferase family (Kmt2a, Kmt2b and Kmt2d). Concomitant to the latter, HERV-W ENV mice displayed increased enzymatic activity of lysine-specific demethylase-1 (LSD1), increased H3K4 mono-methylation, and decreased H3K4 di- and tri-methylation in the hippocampus. Importantly, pharmacological inhibition of LSD1 through oral ORY-1001 treatment normalized abnormal H3K4 methylation and rescued the behavioral and cognitive deficits in HERV-W ENV mice. In conclusion, our study suggests that the expression of HERV-W ENV has the capacity to disrupt various behavioral and cognitive functions and to alter the brain transcriptome in a manner that is highly relevant to neurodevelopmental and psychiatric disorders. Moreover, our study identified epigenetic pathways that may offer avenues for pharmacological interventions against behavioral and cognitive deficits induced by increased HERW-W expression. - Source: PubMed
Publication date: 2025/03/18
Herrero FelisaHeeb CelineMeier MichelleLin Han-YuMueller Flavia SSchalbetter Sina MGruchot JoelWeber-Stadlbauer UlrikeNotter TinaPerron HervéKüry PatrickMeyer Urs - We report eight children with de novo pathogenic DNA variants in chromatin-related genes: MORC2, CHD7, KANSL1, KMT2D, ZMYND11, HIST1HIE, EP300, and KMT2B. All children experienced infection or vaccine-provoked neuroregression or abrupt-onset neuropsychiatric syndromes. Most had delayed development (n = 6) before the first regression, and four had immune deficiency or autoimmunity (n = 4). At a mean age of 4 years 2 months (range 1-8 years), symptoms included infection-provoked autistic/language regression (n = 6), cognitive decline (n = 3), gait deterioration (n = 3), or abrupt-onset anxiety, obsessive-compulsive disorder, and/or tics (n = 5). Three children had ongoing infection-provoked deteriorations. Six children benefited from intravenous immunoglobulin (n = 3) or antibiotics (n = 4). Ribonucleic acid expression of the eight chromatin genes was similar in neuronal, glial, and peripheral leukocytes, unlike non-chromatin neurodevelopmental genes, which have predominantly neuronal expression. These cases demonstrate the role of chromatin dysregulation in autistic regression and abrupt-onset neuropsychiatric syndromes, potentially related to brain and immune gene dysregulation. - Source: PubMed
Publication date: 2025/02/22
Dale Russell CMohammad ShekeebHan Velda XNishida HiroyaGoel HimanshuTangye Stuart GHollway GeorginaTantsis EstherGill DeepakPatel Shrujna