Ask about this productRelated genes to: MAT1A Blocking Peptide
- Gene:
- MAT1A NIH gene
- Name:
- methionine adenosyltransferase 1A
- Previous symbol:
- -
- Synonyms:
- MAT, SAMS, MATA1, SAMS1
- Chromosome:
- 10q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-01
- Date modifiied:
- 2016-10-05
Related products to: MAT1A Blocking Peptide
Related articles to: MAT1A Blocking Peptide
- Aristolochic acid I (AAI) is a potent hepatocarcinogen mainly activated to aristolactam I (ALI). The molecular mechanisms driving ALI‑associated hepatocellular carcinoma (HCC), particularly post‑transcriptional events linking acute liver injury to malignant transformation, remain poorly defined. Here, we integrated pharmacological ALI-target prediction, HCC transcriptomic datasets, weighted gene co-expression network analysis (WGCNA), and SHAP‑based interpretable machine learning to establish a ten-gene signature for ALI-related HCC. Signature dysregulation was validated in a chronic AAI‑carbon tetrachloride (CCL₄) pre-neoplastic mouse model. In vitro phenotypic and molecular responses were investigated in ALI-exposed HepG2 and Huh7 cells, supplemented by molecular docking and 100 ns molecular dynamics simulations. Functional enrichment indicated that core signature genes participate in cell-cycle modulation, metabolic reprogramming, and epigenetic regulation. Consistent upregulation SAE1/AURKA and repressed MAT1A were observed in human HCC and murine pre-neoplastic liver tissues. Acute ALI exposure induced widespread transcription‑translation uncoupling with cell-line-specific patterns. In HepG2, cell-cycle genes were transcriptionally activated without protein elevation, while MAT1A protein increased despite stable mRNA levels. In Huh7, suppressed SAE1/AURKA transcription did not alter protein abundance, and MAT1A protein was reduced with unchanged mRNA expression. Simulations predicted stable ALI binding to SAE1/AURKA but a weak transient the ALI‑MAT1A interaction, explaining the divergent post-transcriptional responses. We propose a biphasic model of ALI hepatotoxicity. Acute ALI induces early post-transcriptional disturbances, whereas chronic AAI injury causes stable signature dysregulation during HCC progression. This signature provides candidate prognostic biomarkers and supports the safety evaluation of aristolochic acid‑containing herbal medicines. - Source: PubMed
Publication date: 2026/09/14
Peng QingHao LiyuanLi ShenghaoWu QinpingYang YingHu Xiaoyu - Bariatric surgery shows variable efficacy in resolving metabolic dysfunction-associated steatohepatitis (MASH), with mechanisms underlying therapeutic heterogeneity remaining unclear. Using multiple male murine MASH models, we demonstrate that vertical sleeve gastrectomy (VSG) ameliorates hepatic steatosis and fibrosis through mechanisms that extend beyond weight loss. Multi-omic profiling reveals VSG enhances hepatic one-carbon metabolism (1CM) via upregulation of methionine adenosyltransferase 1 A (MAT1A), increasing S-adenosylmethionine (SAM) availability and the SAM/SAH ratio. This metabolic reprogramming restores hepatic phosphatidylcholine (PC) /phosphatidylethanolamine (PE) homeostasis, alleviating endoplasmic reticulum stress and mitochondrial dysfunction. Critically, dietary depletion of one-carbon substrates or genetic ablation of MAT1A abolishes VSG's therapeutic effects, while betaine supplementation rescues surgical efficacy. In humans, paired liver biopsies from patients with MASH (n = 4) show MAT1A upregulation correlating with histological improvement, while plasma metabolomics from a separate cohort (n = 42) reveals that patients with poor hepatic response to VSG display compromised one-carbon metabolism signatures, with SAM levels correlating with therapeutic response. These findings establish MAT1A-mediated methylation as an essential mechanism for optimal VSG efficacy in preclinical models and identify one-carbon metabolites as candidate biomarkers for predicting surgical response, suggesting that preoperative metabolic profiling could guide methyl donor supplementation to optimize VSG outcomes in MASH. - Source: PubMed
Publication date: 2026/07/22
Tang BixiShen QiweiYuan JieHuang XianjueShao YikaiZhu NanlinGuo HaoranCao HuiyingWang HanlinWang HanminLi JiaLiu JiaHua RongZang Yi - Perfluorooctanoic acid (PFOA), a persistent environmental pollutant, represents a chronic environmental stressor, yet its role in osteosarcoma progression remains unclear. Here, we integrated network toxicology, machine learning, immune infiltration analysis, single-cell RNA sequencing, molecular docking, molecular dynamics simulation, and in vitro assays to define the mechanisms linking long-term PFOA exposure to osteosarcoma. We identified 28 shared targets between PFOA-associated proteins and osteosarcoma-related genes, which were mainly enriched in oxidative stress, immune regulation, and metabolic reprogramming pathways. Machine learning prioritized nine candidate hub genes, including PNP, SOD2, MAT1A, RELA, PSAT1, CXCL12, PHGDH, PDK4, and CFD, with PHGDH, PSAT1, PDK4, and MAT1A suggesting a metabolism-related axis relevant to PFOA-associated osteosarcoma alterations. Single-cell and immune analyses showed distinct cell-type-specific expression patterns of these genes and their close associations with the tumor immune microenvironment. Molecular docking and molecular dynamics simulations further suggested potential structural compatibility between PFOA and several prioritized hub proteins. Experimentally, prolonged exposure to non-cytotoxic concentrations of PFOA enhanced osteosarcoma cell proliferation and invasion, whereas high concentrations were cytotoxic. Collectively, these findings suggest that long-term PFOA exposure may promote osteosarcoma progression by coupling environmental stress with metabolic reprogramming and immune dysregulation. - Source: PubMed
Publication date: 2026/07/16
Dong YuruZheng JiaxiaoDong XingtongLv YixiaoXu ZixiaYe ChengluoZhu ShuyuanDong HaoruLv Yao - X-rays are a form of ionizing radiation that has sufficient energy to remove electrons from atoms, thereby creating potentially harmful ions. X-ray irradiation during organogenesis can have profound detrimental effects, depending on the developmental stage and irradiating energy. In this study, we examined the impact of X-ray irradiation on zebrafish development at 36 h post-fertilization and observed marked jaw malformation, which was alleviated by folic acid pretreatment. Mechanistic studies revealed that folic acid pretreatment suppressed irradiation-induced production of reactive oxygen species. Transcriptome analysis performed at 24 and 48 h post-irradiation revealed dysregulated expression of apolipoprotein A-IV a (apoa4a), methionine adenosyltransferase 1A (mat1a), heat shock protein 90 alpha class A member 1 tandem duplicate 1 (hsp90aa1.1), FKBP prolyl isomerase 5 (fkbp5), plac8 onzin related protein 3 (ponzr3), and prostaglandin E synthase 3a (ptges3a), which was not observed in zebrafish treated with folic acid before the irradiation. These findings suggest that folic acid alleviates X-ray irradiation-induced jaw malformation in zebrafish, at least in part, by reducing oxidative stress and ameliorating dysregulated gene expression. - Source: PubMed
Das TanishaShiromizu TakashiHiguchi AinaYasojima SakyoMorimoto MisakiHosaka MihoKashima MakotoKoiwa JunkoNishimura Yuhei - Epigenetic alterations play an increasingly recognized role in carcinogenesis and in the development of resistance to anticancer therapies. Epigenetic enzymes (writers and erasers) and effectors (readers) are largely influenced by the availability of metabolites generated through one-carbon metabolism (OCM), the tricarboxylic acid (TCA) cycle, and acetyl-CoA synthesis (ACS). In this study we examined the expression of epigenetic and metabolic genes to investigate their interplay in cholangiocarcinoma (CCA). - Source: PubMed
Publication date: 2026/06/04
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