AATC_RAT Got1 ELISA tesk kit
- Known as:
- AATC_RAT Got1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15645
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- AATC_RAT Got1 ELISA tesk kit
Related genes to: AATC_RAT Got1 ELISA tesk kit
- Gene:
- GOT1 NIH gene
- Name:
- glutamic-oxaloacetic transaminase 1
- Previous symbol:
- -
- Synonyms:
- AST1
- Chromosome:
- 10q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
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- Cellular senescence involves progressive acidification, but how cells sense and adapt to this pH shift remains unclear. Here we report that metabolic enzyme GOT1 functions as a pH sensor that undergoes liquid-liquid phase separation (LLPS) to combat senescence. Proteomic analysis identified GOT1 upregulation in aged human lung cells. Acidic conditions mimicking senescence directly induce GOT1 LLPS via its N-terminal intrinsically disordered region (IDR1), recruiting ME1 to form dynamic enzymatic co-condensates that scavenge reactive oxygen species and alleviate oxidative stress. To quantitatively interrogate GOT1's pH microenvironment during senescence, we engineered BDP-PLP, a first-in-class fluorescent probe conjugating the native GOT1 cofactor pyridoxal phosphate to a BODIPY fluorophore. Operating via a binding-inhibited PET mechanism, this probe enables high-specificity GOT1 targeting and pH-dependent fluorescence lifetime imaging (FLIM). Using FLIM, we achieved quantitative real-time visualization of pH dynamics within GOT1 condensates in living cells, revealing that phase separation generates a highly acidic local microenvironment critical for its anti-senescence function. This study uncovers a pH-triggered phase separation mechanism that bolsters antioxidant defense via metabolic enzyme co-condensation, offering new perspectives on metabolic adaptation in aging and establishing a chemical tool for probing microenvironmental dynamics. - Source: PubMed
Publication date: 2026/09/03
Chen ZiyueLi JiaqiBao YanWang MengmengChen HaoyanZhang MingjiongDing LinaWu ShuangshuangShen Baoxing - Metastasis is the primary cause of treatment failure and adverse prognosis in hepatocellular carcinoma (HCC), and the molecular basis of HCC metastasis remains poorly defined. This work investigated the potential mechanisms underlying HCC metastasis through integrated multi-omics analysis of metabolomics and proteomics. - Source: PubMed
Publication date: 2026/08/19
Wu JingWang JinYu ZhenYang Rui - Sorafenib is a first-line therapy for hepatocellular carcinoma (HCC), but its clinical benefit is limited by significant interpatient variability in response. Identifying reliable candidate biomarkers associated with sorafenib treatment is critical for optimizing treatment strategies and improving patient outcomes. - Source: PubMed
Publication date: 2026/08/05
Zhan MengruLi PenghuiWang WanyiZhao Mingxing - Gut microbial metabolites play crucial roles in regulating systemic immunity, but their mechanisms and limited drug-like properties remain unresolved. Here we report an oral nano-formulation that leverages gut microbial metabolites to modulate T cell metabolism and amplify antitumour immunity. Through an in vitro screening of gut microbial metabolites, we identified 3,4-dihydroxybenzoic acid that improved adoptive T cell therapy and enhanced CD8 T cell stemness by suppressing glycolysis and regulating the Akt-mTORC1-Myc pathway. To harness the potency of 3,4-dihydroxybenzoic acid for systemic cancer immunotherapy, we engineered a 3,4-dihydroxybenzoic acid prodrug nano-emulsion, significantly increasing its oral absorption and half-life. In multiple murine tumour models, the oral nano-emulsion enhanced the expansion of antigen-specific, stem-like CD8 T cells, sensitizing tumours to anti-PD-1 blockade and exerting robust antitumour efficacy. By integrating nanotechnology with microbial-metabolite-based immunotherapy, this study establishes a mechanistic link between the gut microbiota and T cell immunity, offering a promising approach for cancer immunotherapy. - Source: PubMed
Publication date: 2026/08/10
Han KaiCho Young SeokTakahashi MarikoZhou XingwuDobson Hannah EHutchings KimWu YuesongNa YoungseoXie FangCrowther JuliaWu JinmeiXu JinLee ChuanJasewicz HimaniKim YujinNenwani MinalAnimasahun OlamideWuchu FuleiAndren AnthonyWong HarrisonCamp EmmaWan ZiyeWu QiZhang LiXu ChengDong KatherineXu YaoSchwendeman AnnaChen Grace YXie YuyingLyssiotis Costas AClasby MartinNagrath DeepakLei Yu LeoMoon James J - Approximately 90% of patients with pancreatic cancer harbor KRAS mutations, predominantly the KRAS subtype. HRS-4642, a non-covalent inhibitor targeting KRAS, demonstrates potent antitumor efficacy but may ultimately lead to resistance. This study investigates the mechanisms underlying KRAS inhibitor resistance and evaluates strategies to enhance treatment sensitivity. Our findings indicate that a glutamine-restricted diet not only reverses KRAS inhibitor resistance in pancreatic ductal adenocarcinoma (PDAC) but also achieves remission with prolonging survival. Mechanistically, KRAS inhibitor resistance markedly upregulates ANXA1 expression, which, in turn, promotes its binding to the glutamine-related enzyme GOT1 and stabilizes its expression. Additionally, we find that ANXA1 upregulation facilitates mitochondrial localization of GLS1, thereby altering glutamine metabolism. These findings highlight ANXA1-mediated glutamine metabolism as a key driver of KRAS inhibitor resistance and support glutamine-restricted diets as a potential therapeutic strategy for KRAS mutant PDAC. - Source: PubMed
Publication date: 2026/08/06
Li JiatongGu AoJia ZihengLi MengyaoZuo JinluWang ZiyiLi XuechuanFeng JiayiXue TongZhai ShuyangYue ZhuyingAn YangKang SiyuanYuan ZhiqingQiu ShimeiXue YadongLiu LiguoTang NannanLiu Yingbin