Ask about this productRelated genes to: MOGAT2 antibody
- Gene:
- MOGAT2 NIH gene
- Name:
- monoacylglycerol O-acyltransferase 2
- Previous symbol:
- -
- Synonyms:
- MGAT2, DGAT2L5, FLJ22644
- Chromosome:
- 11q13.5
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-14
- Date modifiied:
- 2014-11-19
Related products to: MOGAT2 antibody
Related articles to: MOGAT2 antibody
- GLP-1 therapies for obesity are limited by side effects and weight regain is common after treatment ends. Therefore, alternative treatments with new mechanisms are needed for sustained weight loss. Human MOGAT2 regulates triglyceride metabolism and its inhibition reduces weight in people with obesity, making MOGAT2 a promising target for obesity therapy. - Source: PubMed
Publication date: 2026/04/09
Corbalan J JoseJagadeesan PranaviHuang Chia-YuBeasley James RNickels Joseph T - Hepatitis B virus (HBV) co-opts and interacts with an extensive array of host factors for productive infection. Herein, we develop an HBV reporter virus expressing red fluorescent protein (HBV-RFP) that is suitable for a CRISPR-based genome-wide screen for HBV host dependency factors. HepG2 cells were transduced with a pooled lentiviral library of single-guide RNA (sgRNA) targeting 19,114 human genes, edited and infected with HBV-RFP. RFP-low cells were sorted using fluorescence-activated cell sorting. The sorted cells were expanded and underwent two additional rounds of infection and sorting to enrich for sgRNA-targeted proviral host factors. By next-generation sequencing and bioinformatic analyses, we identified 63 genes as candidate host proviral factors, including known HBV proviral factors: RXRA, POLL, LDLR, and NTCP. Among the novel candidate genes, knockout of 12 genes significantly decreased HBV replication markers. Validation using siRNA knockdown in primary human hepatocytes confirmed several factors including the monoacylglycerol acyltransferase 2 (MOGAT2) gene as a bona fide HBV proviral factor. Further analysis with MGAT2 inhibitors demonstrated that inhibition of MOGAT2 activity impairs HBV transcription and replication. Our study demonstrates the value of the HBV reporter system in identifying previously unrecognized host metabolic factors important for HBV infection, offering a potential avenue for therapeutic development. - Source: PubMed
Publication date: 2025/12/01
Inuzuka TadashiMouzannar KarimZhang MinUmarova ReginaPark Seung BumUchida TakuroMa Christopher DLiang T Jake - Gastric intestinal metaplasia (GIM) is a precancerous lesion that elevates gastric cancer risk. Our prior single-cell RNA sequencing (scRNA-seq) analysis implied aberrant lipid metabolism in GIM. We also established a Ddit4-deficient mouse model that developed severe gastric metaplasia lesions upon Helicobacter pylori (H. pylori) infection. This study aims to define the lipid signatures of metaplasia lesions in gastric carcinogenesis. - Source: PubMed
Publication date: 2025/11/14
Wang HuanLiu SujuanFei XiaoFan WentaoYe YumanXu XinboChen ZhenpingGong XiaominZhou YananWu XidongHe CongLiu JianpingLu NonghuaZhu YinLi Nianshuang - Colorectal carcinogenesis and progression are closely associated with metabolic dysregulation. The role of MOGAT2 in colorectal cancer (CRC) advancement and its underlying metabolic mechanisms remain unclear. This study aimed to explore how MOGAT2 influences tumorigenesis by modulating lipid metabolism. - Source: PubMed
Publication date: 2025/10/27
Jiang ShaofengHe YingJiang JiaruiZhao Xinhan - Obesity significantly increases the risk of hyperlipidemia, type 2 diabetes, and liver disease. This study examined humanized monoacylglycerol acyltransferase 2 mice (HuMgat2) and their response to a high fat diet (HFD) while investigating hepatocyte dysfunction during obesity development. HuMgat2 mice fed a HFD exhibited hyperlipidemia, hyperglycemia, insulin resistance, and metabolic dysfunction-associated steatotic liver disease (MASLD). Elevated levels of cholesterol and triglycerides were associated with increased expression of lipogenic genes and accumulation of nuclear Srebp1/Srebp2. Mice fed a HFD demonstrated impaired insulin signaling and increased glucose production through the expression of gluconeogenesis genes. Liver fibrosis was characterized by collagen deposition and activation of Jak2-Stat3 signaling, resulting in hepatocyte apoptosis. RNA sequencing identified extracellular matrix degradation and apolipoprotein metabolism as being altered. Levels of cytochrome P450 enzymes were downregulated, as indicated by decreased Cyp2b10 and Cyb3a11 levels, alongside reduced expression of the di- and tri-carboxylic acid transporter Slc13a2, correlating with elevated Krebs cycle intermediates. Notably, HuMgat2 mice exhibited responses to a high-fat diet that were comparable to those observed in mMgat2 mice. These findings suggest that HFD consumption and concomitant obesity disrupts metabolite homeostasis, contributing to liver damage and cell death. They also further validate HuMgat2 mice as an excellent preclinical model for testing human MOGAT2 inhibitors as therapeutics for treating obesity. - Source: PubMed
Publication date: 2025/10/15
Corbalan J JoseJagadeesan PranaviNickels Joseph T