L3MBTL2 antibody - C-terminal region (ARP30080_T100)
- Known as:
- L3MBTL2 (anti-) - C-terminal region (ARP30080_T100)
- Catalog number:
- arp30080_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- L3MBTL2 antibody - C-terminal region (ARP30080_T100)
Related genes to: L3MBTL2 antibody - C-terminal region (ARP30080_T100)
- 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 - C-terminal region (ARP30080_T100)
Related articles to: L3MBTL2 antibody - C-terminal region (ARP30080_T100)
- Cachexia is a debilitating muscle-wasting disorder associated with a high mortality rate in cancer patients. However, the molecular mechanisms of muscle contractile dysfunction underlying cancer-induced cachexia (CIC) remain poorly characterized. Here, we demonstrated that CIC reorients global SUMOylation in skeletal muscle cells and alters the stability of various SUMO machinery components, particularly SUMO isopeptidases. The non-canonical polycomb repressor protein L3mbtl2 was among the predominant proteins with enhanced SUMOylation level in CIC. Surprisingly, in contrast to previous notions, we found that L3mbtl2 activates transcription of a large cohort of genes regulating muscle contraction. Mechanistically, L3mbtl2 associates with Ash2L, a component of the SET1/MLL histone methyltransferase complex. Increased SUMO modification of L3mbtl2 in CIC leads to partitioning of Ash2L from its target genes, resulting in impaired calcium handling, sarcomere disorganization and impeded muscle cell contractile properties. Our findings reveal an unprecedented connection between SUMO and CIC, a paradoxical SUMO-associated transcriptional activator function of L3MBTL2 and hold potential for developing therapeutic interventions to ameliorate CIC. - Source: PubMed
Publication date: 2026/09/09
Gand Luis VincensLi MugengBrandt KatharinaZhou BaoyuNassar-Grioua AmelGondin JulienBecker EdgarPich AndreasKraft TheresiaAmrute-Nayak MamtaNayak Arnab - Epigenetic-related genes (ERGs) play a pivotal role in cancer development and progression. However, their potential for cervical cancer (CC) diagnosis and prognosis remains underexplored. - Source: PubMed
Publication date: 2026/07/03
Lin XuefenZheng JianfengLi YanhongWang SipingLiu QinyingChen LijunLi SangSun Yang - BACKGROUND: 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. METHODS: We employed two TWAS frameworks to integrate multi-tissue expression quantitative trait loci (eQTL) data from GTEx v8 with a TN genome-wide association study (GWAS). Candidate loci were systematically validated through a multi-tiered analytical cascade, encompassing MR, summary-based MR (SMR), Bayesian co-localization, and replication across four independent cohorts (BrainMeta v2, PsychENCODE, eQTLGen, and Westra blood). Cell-type specificity was mapped using gsMAP analysis. Besides, a rat model of TN was established to validate the expression of the target. In addition, to elucidate shared risk factors, two-sample analysis quantified the role of Risk-Gene pathways. Finally, phenome-wide association studies (PheWAS) was performed to interrogate potential off-target effects of prioritized therapeutic targets using FinnGen R10 data. Analytical robustness was ensured via sensitivity analyses and Cochran’s Q heterogeneity testing. RESULTS: TWAS prioritized L3MBTL2 as a Multi-tissue regulator, showing consistent protective effects across tissues (OR range 0.56–0.82; smallest P = 9.13 × 10− 14) validated by MR, SMR and co-localization (posterior probability > 0.8), leading to its designation as Tier 1. In contrast, CIDEA (Tier 2) exhibited tissue-specific risk in esophageal mucosa (β = 0.42, FDR P = 0.0046) but lacked cross-tissue reproducibility. gsMAP analysis revealed spatial enrichment of TN-associated cells in tissues, including the epidermis. TN animal experiments showed lower expression of L3MBTL2 in the hypothalamic region, confirming our genomic findings. Finally, risk factor analysis identified basal metabolic rate as a shared risk factor for both reduced L3MBTL2 expression and increased TN risk. PheWAS analysis indicated that therapeutic targeting of L3MBTL2 may elicit adverse effects, specifically obesity-related phenotypes and benign uterine fibroids. CONCLUSIONS: This study identifies L3MBTL2 as a high-confidence candidate gene for TN, with experimental evidence supporting its role in the hypothalamus. These findings provide novel insights into TN pathophysiology and suggest that L3MBTL2 warrants further investigation as a potential therapeutic target. - 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