MAT2A Antibody
- Known as:
- MAT2A Antibody
- Catalog number:
- XW-8062
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- MAT2A Antibody
Related genes to: MAT2A Antibody
- Gene:
- MAT2A NIH gene
- Name:
- methionine adenosyltransferase 2A
- Previous symbol:
- -
- Synonyms:
- SAMS2, MATA2, MATII
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-01
- Date modifiied:
- 2016-01-27
Related products to: MAT2A Antibody
Related articles to: MAT2A Antibody
- Cancer progression is closely associated with metabolic reprogramming and immune evasion. Extracellular adenosine (eADO) metabolism regulates adenosine receptor activation within the tumor microenvironment (TME). Predominantly through the adenosine A2A receptor (A2AR), and in some contexts through the adenosine A2B receptor (A2B receptor), eADO signaling suppresses antitumor immune responses and contributes to resistance to immunotherapy. Production of eADO is largely driven by ecto-5'-nucleotidase (CD73), which catalyzes the conversion of eADO monophosphate (AMP) into eADO. In parallel, methylthioadenosine phosphorylase (MTAP) deletion - frequently co-occurring with loss of cyclin-dependent kinase inhibitor 2A (CDKN2A) does not increase eADO levels but instead leads to intracellular accumulation of methylthioadenosine (MTA) reshaping methylation homeostasis and creating selective metabolic dependencies involving protein arginine methyltransferase 5 (PRMT5) and methionine adenosyltransferase 2A (MAT2A). Recent evidence further indicates that nucleoside transport dynamics, particularly via equilibrative nucleoside transporter 1 (ENT1), regulate intracellular adenosine (iADO) availability in T cells and represent an additional regulatory layer linking extracellular purinergic signaling with intracellular immunometabolic control. Accordingly, we propose a functional immunometabolic convergence framework in which CD73-dependent extracellular eADO signaling, ENT1-regulated iADO handling, and MTAP loss-associated metabolic rewiring function as parallel yet cooperative processes that stabilize tumor immune escape. - Source: PubMed
Publication date: 2026/05/02
Rosa Vandriel Pedone daFontana MichelliRichter Schmitz Carine RaquelBuzatto Maike ValentimGiacomelli Iuri RaielRoman Junior Walter AntônioBoison DetlevBagatini Margarete DulceOliveira Maciel Sarah Franco Vieira de - Methionine addiction is a fundamental and general hallmark of cancer cells. Recombinant (rMETase) degrades extracellular methionine. rMETase, or other means of restricting methionine, in combination with numerous types of chemotherapy have shown synergistic cancer-selective efficacy. AG-270, a methionine adenosyltransferase 2A (MAT2A) inhibitor, blocks intracellular conversion of methionine to S-adenosylmethionine (SAM), the central reaction of the methionine cycle. The present study aimed to evaluate the synergistic and cancer-selective efficacy of the combination of AG-270 and rMETase in a co-culture model of cancer and normal cells. - Source: PubMed
Publication date: 2026/05/01
Kim JinsooHan QinghongLi ShukuanKang Byung MoMizuta KoheiAsano YoheiMiyashi YutaBouvet MichaelHoffman Robert M - In cancers with deletions, MAT2A inhibition has emerged as a promising therapeutic strategy in cancer treatment through a synthetic mechanism. Herein, we report the design and optimization of a novel series of pyridazinone-based MAT2A inhibitors via a ring-opening strategy from . Through iterative structure-activity relationship (SAR) studies, compound was identified as the lead compound, displaying potent MAT2A inhibition (IC = 17.5 nM) and strong cellular activity in HCT-116 MTAP KO cells (GI = 0.76 μM). Moreover, retained high potency in -naturally deficient cancer cell lines. , demonstrated favorable pharmacokinetic properties and induced pronounced antitumor efficacy in the NCI-H838 xenograft model with minimal toxicity. Mechanically, treatment with markedly reduced SAM and sDMA levels both and Collectively, these results establish pyridazinone as a privileged scaffold for MAT2A inhibition and identify compound as a compelling lead for further preclinical development. - Source: PubMed
Publication date: 2026/04/23
Zhang YuWang PengfeiXie ZhichengHuang YilunDing YaqiLiu JiaChen YiHu Youhong - Homozygous loss of the 9p21 locus encompassing CDKN2A, CDKN2B, and MTAP is the most frequent copy number alteration across tumor types, making it a promising target for precision medicine strategies. To explore drug vulnerabilities exposed by this loss, we generated 9p21 locus isogenic bladder cancer (BLCA) cell models to perform a multiparametric drug screen, testing 2,349 compounds. We identified cytarabine and methotrexate as significantly more effective in the 9p21 compromised BLCA cells. Analysis of morphological alterations further supported a genotype-specific activity of nucleoside analogs, nominating gemcitabine as a drug with greater efficacy in this context. To further exploit MTAP loss, we explored drug combinations targeting MTAP synthetic lethal partners, PRMT5 and MAT2A. Synergy between cytarabine and inhibitors of PRMT5 (MRTX1719) and MAT2A (AG-270) was mediated by a differential activation of DNA damage and replication stress markers, suggesting an exploitable vulnerability. In fact, rational drug combinations with ATR/CHK1 pathway inhibitors increased efficacy while maintaining 9p21-specificity. Finally, we confirmed the effectiveness of these combinations in cell models of pancreatic adenocarcinoma and pleural mesothelioma, two tumor types with high prevalence of MTAP loss and, most notably, in bladder cancer patient-derived organoids, underscoring the strong translational potential of our findings. - Source: PubMed
Publication date: 2026/04/18
Bevilacqua RiccardoGasperini PaolaCantore ThomasMacedo-Silva CatarinaPancher MichaelRadić MartinaYue HaiyanQuaini OrsettaFedrizzi TarcisioGatto PamelaSeiler RolandKiss BernhardAdami ValentinaLorenzin FrancescaKruithof-de Julio MariannaFaltas Bishoy MorrisDemichelis Francesca - Major depressive disorder (MDD) lacks reliable laboratory tests for diagnosis and treatment monitoring, underscoring the need for robust molecular readouts in blood. Beyond symptom-based classification, MDD can also be viewed as a condition involving impaired homeostatic regulation across stress-responsive, immune, metabolic, and neural systems. Consistent with this perspective, altered intron retention (IR) patterns have been observed in peripheral blood in depression-related and treatment-response contexts, supporting the translational relevance of this RNA-processing layer to mood disorders. A key observation underpinning this review is that IR can function as a reversible, intervention-responsive readout of physiological state. In a pre-symptomatic stress-like state in klotho mutant mice (a premature-aging model), widespread IR increases revert toward a healthy pattern upon treatment, suggesting that IR is embedded in a controllable homeostatic layer. Against the backdrop of limited cross-cohort transferability of differential gene expression (DGE) signatures, we propose that IR provides a mechanistically grounded biomarker layer because it reports regulated RNA processing states rather than context-fragile abundance endpoints. We operationalize IR as a post-transcriptional "throttle" on effective gene output, with increased IR/detained intron (DI) states acting as a reversible brake and decreased IR acting as an accelerator that increases translation-competent mRNA supply. Mechanistic exemplars across immune, metabolic, and neuronal systems (e.g., IFNG, OGT, MAT2A, neuronal activity-triggered intron excision, and intron detention-mediated stemness/differentiation switching in adult neural stem cells) show that defined inputs can switch IR/DI states to tune output kinetics. Integrating these findings, we propose an "Intron Retention Homeostat" (IR-Homeostat) model in which cells sense deviations from physiological set points and implement feedback control of gene output through switchable IR/DI regulation. This framework positions IR not only as a robust state readout for stratification, treatment response prediction, and pharmacodynamic profiling, but also as a tractable entry point to identify the molecular sensors and mediators that couple homeostatic signals to RNA processing control. - Source: PubMed
Publication date: 2026/03/30
Okada NorihiroMaruko AkikoOshima KenshiroNishi AkinoriKobayashi Yoshinori