L3MBTL2 antibody - N-terminal region (ARP30081_P050)
- Known as:
- L3MBTL2 (anti-) - N-terminal region (ARP30081_P050)
- Catalog number:
- arp30081_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- L3MBTL2 antibody - N-terminal region (ARP30081_P050)
Related genes to: L3MBTL2 antibody - N-terminal region (ARP30081_P050)
- Gene:
- L3MBTL2 NIH gene
- Name:
- L3MBTL histone methyl-lysine binding protein 2
- Previous symbol:
- -
- Synonyms:
- H-l(3)mbt-l, DKFZP761I141, dJ756G23.3
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-29
- Date modifiied:
- 2019-01-22
Related products to: L3MBTL2 antibody - N-terminal region (ARP30081_P050)
Related articles to: L3MBTL2 antibody - N-terminal region (ARP30081_P050)
- Trigeminal neuralgia (TN) is a neurological disorder affecting the maxillofacial region. Current treatment relies on pharmacotherapy and invasive interventions; however, the growing prevalence of drug-resistant cases highlights the need for a mechanistic understanding and novel biomarkers. In the present study, transcriptome-wide association study (TWAS) and Mendelian randomization (MR) approaches were adopted to identify priority causative genes and therapeutic targets, thereby bridging the gap in our understanding of the polygenic etiology and tissue-specific pathophysiology of TN. - Source: PubMed
Publication date: 2025/12/11
Wang HongweiHuang MinHuang YiHu KaimingHuang YunqinLiang TaoYao Jinguang - Undefined epigenetic programs act to probabilistically silence individual autosomal alleles, generating unique individuals, even from genetic clones. This random monoallelic expression can explain variation in traits and diseases that differences in genes and environments cannot. Here, we developed the nematode Caenorhabditis elegans to study monoallelic expression in whole tissues, and defined a developmental genetic regulation pathway. We found maternal H3K9 histone methyltransferase (HMT) SET-25/SUV39/G9a works with HPL-2/HP1 and LIN-61/L3MBTL2 to randomly silence alleles in the intestinal progenitor E-cell of 8-cell embryos to cause monoallelic expression. SET-25 was antagonized by another maternal H3K9 HMT, MET-2/SETDB1, which works with LIN-65/ATF7IP and ARLE-14/ARL14EP to prevent monoallelic expression. The HMT catalytic SET domains of both MET-2 and SET-25 were required for regulating monoallelic expression. Our data support a model wherein SET-25 and MET-2 regulate histones during development to generate patterns of somatic monoallelic expression that are persistent but not heritable. - Source: PubMed
Publication date: 2025/11/28
Sands BryanYun Soo ROshima JunkoMendenhall Alexander R - Stomach adenocarcinoma (STAD) exhibits high molecular heterogeneity and poor prognosis, necessitating robust biomarkers for risk stratification. While SUMOylation, a post-translational modification, regulates tumor progression, its prognostic and immunological roles in STAD remain underexplored. - Source: PubMed
Publication date: 2025/08/01
Luo KaipingXing DonghuiHe XiangZhai YixinJiang YananZhan HongjieZhao Zhigang - Small Ubiquitin-like MOdifier-mediated modification (SUMOylation) is associated with sepsis; however, its molecular mechanism remains unclear. Herein, hub genes and regulatory mechanisms in sepsis was investigated. The GSE65682 and GSE95233 datasets were extracted from public databases. Differential analysis and Weighted Gene Co-expression Network Analysis (WGCNA) were conducted in GSE65682 to identify differentially expressed genes (DEGs) and key module genes. Candidate genes were derived by intersecting with SUMOylation-related genes (SUMO-RGs). The Least Absolute Shrinkage and Selection Operator (LASSO) and Support Vector Machine-Recursive Feature Elimination (SVM-RFE) were utilized to identify significant feature genes. The convergence of those genes was utilized for diagnostic assessment and expression validation. Hub genes were defined as those exhibiting an area under the curve (AUC) greater than 0.7, significant gene expression, and a consistent trend. Localization and functional analyses of hub genes were conducted to enhance the understanding of these genes. Immune analysis, regulatory network construction, and drug prediction were performed. Six hub genes were identified: RORA, L3MBTL2, PHC1, RPA1, CHD3, and RANGAP1. These genes possessed considerable diagnostic significance for sepsis and were also markedly downregulated in the condition. Hub genes were predominantly enriched in the ribosome pathway and exhibited a strong correlation with differential immune cells. Activated CD8 + T cells exhibited a positive correlation with RORA. Based on the predicted and established regulatory network, AC004687.1 was observed to modulate PHC1 expression via hsa-miR- 142 - 5p. A total of six hub genes (RORA, L3MBTL2, PHC1, RPA1, CHD3, and RANGAP1) associated with SUMOylation was identified in sepsis in the current study. The findings are likely to aid in the differentiation between control and disease states, offering substantiation for the diagnosis of sepsis. - Source: PubMed
Publication date: 2025/04/24
Teng XueWang QiMa JinlingLi Dongmei - Wound healing (WH) poses a significant socio-economic burden due to its high incidence and recurrence rates. Iron overload (IO) could be a factor leading to delayed WH. This study thus analyzed IO-related genes (IORGs) in WH, offering possibilities for developing new therapeutic strategies. Differential gene expression (DEGs) analysis was conducted between the WH group and intact skin (IS) group, intersected with IORGs to obtain differentially expressed IORGs (DE-IORGs). Functional enrichment analysis and potential drug screening were performed on DE-IORGs. A protein-protein interaction (PPI) network of DE-IORGs was constructed, and hub genes were identified using CytoHubba and MCODE methods. ROC curves of hub genes were plotted, and their expression levels in WH and IS groups as well as inter-gene correlations were analyzed. Additionally, immune infiltration variances in WH and IS groups, along with miRNA and TFs of hub genes, were examined. Finally, the effect of EGFR on skin wound healing was verified by scratch healing assay. 39 DE-IORGs were predominantly enriched in signaling pathways like HIF-1 signaling pathway and Th17 cell differentiation. Potential drugs for treating WH (e.g., felbamate, SA-94315, GANT-58, rucaparib) were identified. Three hub genes related to IO in WH were pinpointed (HIF1A, CDKN2A, EGFR) with diagnostic value. Immune infiltration analysis showed higher levels of immune cells like endothelial cells and macrophages in the WH group. Additionally, 55 miRNAs (e.g., hsa-mir-200a-3p, hsa-mir-218-5p) and 2 TFs (L3MBTL2, ZNF76) regulating the three hub genes were predicted. Cell experiments showed that EGFR could promote skin wound healing. The study suggested HIF1A, CDKN2A, and EGFR as potential diagnostic biomarkers for effective WH diagnosis, offering new insights into identifying potenti1al therapeutic targets for WH treatment. - Source: PubMed
Publication date: 2025/04/19
Peng YinboSheng JuxiangLiu TiantianHe RuizheXu Peng