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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- Non-small cell lung cancer (NSCLC) remains one of the most lethal malignancies globally, largely due to its asymptomatic early course and poor prognosis at advanced stages. The rapid proliferation of NSCLC cells drives an increased demand for bioenergy and biosynthetic precursors, which is met through metabolic reprogramming. Targeting this reprogramming to cut off the energy for tumors therefore represents a promising therapeutic strategy for NSCLC. - Source: PubMed
Publication date: 2026/07/09
Chen ZixuanChen ZiyuanGe ZhenLiu JiayuanFang ShuaiChen WeiHong ZhiqiSheng YufeiZhao XiaodongHu WentaoZhou Chengwei - Pancreatic ductal adenocarcinoma has a unique tumor microbiome, and the depletion of gut bacteria or fungi using antibiotic/antifungal cocktails has been shown to decrease pancreatic tumor burden in mice. However, functional studies evaluating the role of tumor-associated microbes are few due to the limited availability of clinically relevant microbiota. Here, we describe in detail an effective workflow for the isolation of bacteria and fungi from the duodenum and tumor of pancreatic cancer patients, specifically optimized for cryopreserved, low biomass samples. Using this workflow we also isolated microbiota from normal pancreatic tissue and duodenum from organ donors, and we confirmed the presence of bacteria and fungi isolated from tissue samples with 16S and ITS sequencing analysis. Isolation and sequencing results show distinct similarities between the pancreatic and duodenal microbiomes and highlight unique bacterial strains that survive in the tumor microenvironment. As a proof of concept, we characterized a select strain () isolated from a pancreatic tumor, using whole genome sequencing, metabolomics, and tumor cultures to determine its potential impact on the pancreatic tumor microenvironment. In summary, this optimized workflow allows for the isolation of a variety of bacteria and fungi from low biomass, cryopreserved pancreatic and duodenal tissues, which can then be used for functional studies characterizing clinically relevant tumor-associated microbiota. - Source: PubMed
Publication date: 2026/07/07
Awad DominikAttebury HollyHong RyanKim KwiZhang LiBischoff AllisonAchi SajandenDekker AaronLesniak NickThe StephanieNieto Carrion Joseph ANelson Noah SStrayhorn ChristopherGriffith Brian DWatkoske Hannah REspinoza Carlos EPeterson NicoleLenard MirandaMuir AlexanderSahai VaibhavLi GenFrankel Timothy LPasca di Magliano MarinaLyssiotis Costas ASchmidt Thomas MDaley Donnele - Lung adenocarcinoma (LUAD) is a highly aggressive cancer with limited treatment options. This study investigated key genes linking ferroptosis and amino acid metabolism in LUAD using bioinformatics and experimental validation. Analysis of TCGA and GEO datasets identified GOT1 (upregulated) and CDO1 (downregulated) as core regulators. High GOT1 expression was associated with advanced clinicopathological characteristics and poor survival (log-rank P < 0.05). Functional studies demonstrated that GOT1 knockdown suppressed LUAD cell proliferation and clonogenic growth while promoting apoptosis, and also reduced tumor growth in vivo (P < 0.001). In addition, CDO1 showed an expression pattern consistent with a potentially protective role in LUAD and was inversely correlated with GOT1 (Spearman's R = - 0.177, P < 0.001). Finally, a prognostic model incorporating GOT1 showed strong predictive accuracy (C-index = 0.705). These findings highlight the important role of GOT1 in LUAD progression and suggest that it may contribute to ferroptosis-related amino acid metabolic reprogramming, supporting its potential as a prognostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/07/06
Li WenWu RuiyueChen XiGuo JuanjuanJian ShengqiangSu FeiYuan FangyunLu YongbinZhao DaZhang TaoHou Xiaoming - Acetaminophen (APAP)-induced acute liver injury (AILI) is a prevalent clinical liver condition caused mostly by oxidative stress and mitochondrial damage. Dental pulp stem cells (DPSCs) possess antioxidant, anti-inflammatory, and immunomodulatory capabilities, demonstrating significant potential in liver diseases. However, during in vitro culture, they are typically maintained under normoxic conditions (21% O), which is very different from the hypoxic oxygen level that is found in vivo. It remains unclear whether hypoxic-conditioned dental pulp stem cells (Hyp-DPSCs) exhibit superior therapeutic effects compared to normoxic-conditioned dental pulp stem cells (Nor-DPSCs). This study demonstrated that 24-h exposure to 1% O significantly enhanced HIF1A/HIF-1α expression in DPSCs. It promoted mitophagy through the MYC-HIF1A-BNIP3 pathway, enhancing mitochondrial shape and function while reducing oxidative stress in DPSCs. Furthermore, in vitro and in vivo experiments demonstrated that Hyp-DPSCs were far more potent than Nor-DPSCs in boosting the expression of hepatic antioxidant factors and enhancing macroautophagy/autophagy to reduce AILI. These findings revealed that hypoxia activated mitophagy in DPSCs, enhancing their therapeutic efficacy against AILI and providing a novel strategy for stem cell-based AILI treatment.: AILI: acetaminophen-induced acute liver injury; ANOVA: analysis of variance; APAP: acetaminophen; BAX: BCL2 associated X, apoptosis regulator; BCL2: BCL2 apoptosis regulator; BNIP3: BCL2 interacting protein 3; BNIP3L: BCL2 interacting protein 3 like; CASP3: caspase 3; CAT: catalase; CCK-8: cell counting kit-8; CM: conditioned medium; COX4I1: cytochrome c oxidase subunit 4I1; CPT1A: carnitine palmitoyltransferase 1A; CQ: chloroquine; DPSCs: dental pulp stem cells; ELISA: enzyme-linked immunosorbent assay; GO: Gene Ontology; GOT1/AST: glutamic-oxaloacetic transaminase 1; GPT/ALT: glutamic - pyruvic transaminase; GPX4: glutathione peroxidase 4; GSH: glutathione; Hyp-DPSCs: hypoxic-conditioned dental pulp stem cells; H&E: hematoxylin and eosin; HIF1A/HIF-1α: hypoxia inducible factor 1 subunit alpha; HMOX1/HO-1: heme oxygenase 1; HUVECs: human umbilical vein endothelial cells; IF: immunofluorescence; IHC: immunohistochemistry; IL1B/IL-1β: interleukin 1 beta; IL6: interleukin 6; i.p.: intraperitoneally; i.v.: intravenous injection; KEGG: Kyoto Encyclopedia of Genes and Genomes; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MSCs: mesenchymal stem cells; MYC: MYC proto-oncogene, bHLH transcription factor; NAC: N-acetylcysteine; NAPQI: N-acetyl-p-benzoquinone imine; NFE2L2/NRF2: NFE2 like bZIP transcription factor 2; Nor-DPSCs: normoxic-conditioned dental pulp stem cells; PRKN/parkin: parkin RBR E3 ubiquitin protein ligase; PLIN2: perilipin 2; PINK1: PTEN induced kinase 1; PPARA/PPARα: peroxisome proliferator activated receptor alpha; PPARG/PPARγ: peroxisome proliferator activated receptor gamma; ROS: reactive oxygen species; SEM: standard error of the mean; SOD1: superoxide dismutase 1; SQSTM1/p62: sequestosome 1; TEM: transmission electron microscopy; TNF/TNF-α: tumor necrosis factor; TOMM20: translocase of outer mitochondrial membrane 20; VDAC1: voltage dependent anion channel 1; WB: western blot. - Source: PubMed
Publication date: 2026/07/05
Li JunyiYang QianyuPang PengchengLiu YeLiu XiaojingZhong WanyangZhang RuiSun WenaoHe YanYe Qingsong - Small intestinal neuroendocrine tumors (SI-NETs) are slow-growing but highly metastatic, with most patients presenting metastases at diagnosis. Radical surgery remains the only potential curative option when feasible. Consequently, there is a critical need for novel therapeutic strategies that can limit tumor progression and enable more personalized treatment approaches in combination with current clinical practices. In this study, we evaluated the impact of metformin on SI-NET cell growth in vivo, characterized the associated microRNA expression profile, and identified potential driver genes modulated by metformin treatment. - Source: PubMed
Publication date: 2026/06/25
Axling FredrikBackman SamuelHellman PerNorlén OlovBarazeghi ElhamStålberg Peter