Got2
- Known as:
- Got2
- Catalog number:
- 039150A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Got2
Related genes to: Got2
- Gene:
- GOT2 NIH gene
- Name:
- glutamic-oxaloacetic transaminase 2
- Previous symbol:
- -
- Synonyms:
- mitAAT, KATIV, KAT4, KYAT4
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-04-26
Related products to: Got2
Related articles to: Got2
- Glioblastoma is the most aggressive primary brain tumor in adults, with limited therapeutic success and, therefore, poor prognosis. Its malignancy is partly driven by the high proliferative capacity of glioblastoma cells, yet the underlying molecular mechanisms remain unclear. Recent studies have revealed transcriptomic similarities between glioblastoma cells and human fetal neural stem/progenitor cells (NSCs), suggesting that glioblastoma may exploit developmental programs that promote NSC proliferation. Fetal human NSCs rely on glutaminolysis-a metabolic pathway induced by the human-specific mitochondrial protein ARHGAP11B-to sustain proliferation. Here, we show that ARHGAP11B expression correlates with glioma malignancy and is essential for glioblastoma cell proliferation, implicating a critical role of glutaminolysis in tumor growth. Among glutaminolysis-related enzymes, glutamic-oxaloacetic transaminase 2 (GOT2) shows a strong positive correlation with glioma grade and poor patient prognosis. Functional assays reveal that GOT2 knockdown significantly suppresses glioblastoma cell growth, indicating that GOT2-mediated glutaminolysis is critical for their proliferation. Metabolomic profiling further shows that GOT2 is required for nucleotide precursor synthesis, underscoring its role in supporting DNA replication. Consistently, GOT2 depletion reduces the proportion of glioblastoma cells in the S phase of the cell cycle. These findings suggest glioblastoma cells hijack an evolutionarily adapted metabolic program to support malignant growth. - Source: PubMed
Publication date: 2026/05/13
Bespalov Maxim MGkini VasilikiIloglu ZeynepYamada SeiyaNemoto AkiraFilppu PauliinaTrontti KaleviAndriichuk LiliiaPietiläinen OlliLe Joncour VadimNieminen Anni ILaakkonen PirjoNamba Takashi - Glucose deprivation is a major metabolic stress that requires coordinated adaptive responses to maintain cellular homeostasis and survival, yet the role of tripartite motif-containing 24 (TRIM24) in this process remains unclear. To address this question, we generated CRISPR-Cas9-mediated TRIM24-knockout MCF-7 and HEK293 cell lines, performed targeted metabolomic profiling and aspartate assays, used 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR), aminooxyacetic acid (AOA), aspartate supplementation, and glutamic-oxaloacetic transaminase 2 (GOT2) knockdown to probe AMPK signaling and aspartate metabolism, and examined starvation responses in constitutive Trim24 knockout mice on a C57BL/6 background. Loss of TRIM24 sensitized cells to glucose deprivation. Re-expression of TRIM24 partially restored cell viability under glucose deprivation in both MCF-7 and HEK293 cells. Under glucose-free conditions, TRIM24 deficiency was associated with impaired AMP-activated protein kinase (AMPK) pathway activation, increased intracellular aspartate accumulation, and altered ATP/AMP levels. Pharmacological reactivation of AMPK by AICAR improved the survival of TRIM24-deficient cells under glucose deprivation. Reducing intracellular aspartate by AOA treatment or GOT2 knockdown restored AMPK pathway activation and improved adaptation to glucose deprivation, whereas exogenous aspartate suppressed AMPK signaling and increased ATP/AMP levels. In vivo, starvation of Trim24-deficient mice was associated with reduced AMPK pathway activation and increased aspartate levels. Together, these findings support a model in which TRIM24 contributes to adaptation to glucose deprivation and in which abnormal aspartate accumulation contributes to impaired AMPK pathway activation in TRIM24-deficient cells. - Source: PubMed
Publication date: 2026/04/14
Yu XiaochenAn DuopengRen DaduiHe PengYang YunkaiChen NanyeWang RuiWu ShanFeng JunFeng Meiqing - Anoectochilus roxburghii (A. roxburghii) is a valuable herb in traditional Chinese medicine, valued for its medicinal properties. Wild A. roxburghii is rare and requires specific environmental conditions, making artificial cultivation challenging. High-temperature acclimation in plants - physiological and biochemical adjustments to tolerate elevated temperatures - has practical applications in agriculture. Our previous study showed that high-temperature acclimation enhances the heat tolerance of the A. roxburghii accession 'Meihuashan', though the molecular basis remains unclear. In this study, we conducted transcriptomic and metabolomic analyses on control (CK), 3-day high-temperature acclimated (T1, 35°C), and 4-day high-temperature acclimated (T2, 35°C) 'Meihuashan' plants. RNA sequencing identified 79,086 unigenes and 12,404 protein-coding genes. Gene ontology and pathway enrichment analyses revealed that metabolic pathways were significantly enriched in the high-temperature response. Subsequent untargeted metabolomic analysis detected 1014 metabolites in the high-temperature treatment group, with 157 differentially expressed metabolites. Orthogonal partial least square-discriminant analysis revealed differentially expressed metabolites associated with flavone, phenylpropanoid, and alkaloid biosynthesis, along with amino acid, lipid, and carbohydrate metabolism. Integrated analysis further highlighted the central role of the carbon fixation pathway, in which key enzyme-encoding genes (e.g. PCK1, GOT2, ALDOA, TPI1) and their corresponding metabolites exhibited significant co-variation under high-temperature stress. These findings suggest that metabolic changes involving amino acids, lipids, and carbohydrates may play a key role in the high-temperature acclimation of 'Meihuashan'. - Source: PubMed
Zhang ShuheLi HaimingZou HuiLi HepingLin JiangboDai Yimin - Photoreceptor (PR) loss causes vision loss in many blinding diseases, and effective therapies to prevent this cell loss are lacking. Aspartate aminotransferases (GOTs), located in the cytosol (GOT1) and mitochondria (GOT2), are key components of the malate-aspartate shuttle, which transfers reducing equivalents from cytosol to mitochondria. Previous work has implicated the GOTs as potential modulators of blinding retinal disease. To determine the roles of GOT1 and GOT2 in rod PRs, we generated rod PR-specific or conditional knockout mice ( or cKO). We previously showed that cKO causes PR degeneration and is accompanied by NADH accumulation and a decreased retinal NAD/NADH ratio. Here, we show that NADH oxidation via metabolic or genetic means prolongs PR survival in cKO animals, implicating NADH accumulation, or reductive stress, as a key driver of PR degeneration. In contrast, cKO causes minimal PR degeneration and alterations in retinal NADH and the NAD/NADH ratio that oppose reductive stress. Interestingly, GOT2, but not GOT1, is decreased in multiple models of PR degeneration, including retinal detachment (RD) where the NAD/NADH ratio favors a reductive state. Notably, loss of in PRs demonstrates a neuroprotective effect after experimental RD suggesting decreased GOT2 expression may be part of a stress response to promote PR survival. Overall, this study illustrates the differential dependence on the GOTs for PR health, provides evidence that an overly reductive environment is detrimental to PR survival, and identifies GOT2 as a novel therapeutic target with potentially broad application in blinding diseases. - Source: PubMed
Publication date: 2026/04/07
Chen MeiniWeh EricGoswami Moloy TWeh Katherine MHager HeatherSajjakulnukit PeterWeingarten AviSubramanya ShubhaMiller NicholasChaudhury SraboniPiraino EmmaChandel Navdeep SRyals Renee CLyssiotis Costas AWubben Thomas J - Glucose is an important fuel in cancer cells, however, its availability may be limited in solid tumors. Cell-autonomous, metabolic adaptations of cancer cells and non-malignant cells to glucose deprivation are still incompletely understood. - Source: PubMed
Publication date: 2026/03/03
Konrad BarbaraBluemel GabrieleHaitzmann TheresaFrech TobiasVandekeere AnkePlanque MélanieBubalo VisnjaSchindlmaier KatharinaJäger VanessaDengler Michael AStryeck SarahBrcic LukaLindenmann JörgStiegler PhilippBresilla DoruntinaMadreiter-Sokolowski Corina TMadl TobiasEichmann Thomas OKneidinger NikolausFendt Sarah-MariaLeithner Katharina