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Our results suggested that glutamine (show GFPT1 ELISA Kits) metabolism is involved in the pathogenesis of rheumatoid arthritis and that GLS1 plays an important role in regulating rheumatoid arthritis fibroblast-like synoviocyte proliferation
Gls2 (show GLS2 ELISA Kits) expression is regulated by the dietary protein/carbohydrate ratio. This effect was not observed in Ppara (show PPARA ELISA Kits)-null mice.
studies show that the formation of large GAC oligomers is not a pre-requisite for full enzymatic activity. They also offer a mechanism by which the binding of activators like inorganic phosphate enables the activation loop to communicate with the active site to ensure maximal rates of catalysis, and promotes the opening of the lid to achieve optimal product release.
Conformational changes in the activation loop of mitochondrial glutaminase C: A direct fluorescence readout that distinguishes the binding of allosteric inhibitors from activators.
findings suggest that glutaminase Heterozygote mice have a pro-cognitive profile in the trace fear conditioning paradigm, and this phenotype involves activation of both hippocampus and Anterior Cingulate Cortex.
studies demonstrate that GLS is required for tumorigenesis and support small molecule and genetic inhibition of GLS as potential approaches for targeting the tumor cell-autonomous dependence on GLS for cancer therapy.
The Phosphate-Activated Glutaminase (show GLS2 ELISA Kits)(PAG (show PRDX1 ELISA Kits)) is mainly active in mouse kidney, brain and liver, and shows different kinetics depending on which type of PAG (show PRDX1 ELISA Kits) is expressed.
The network identified in glutaminase deficient fetal mouse brain involves (a) cellular assembly and organization and (b) cell signaling and cell cycle, suggesting that Gls is crucial for neuronal maturation.
kidney-type glutaminase (KGA) as a novel partner of Bmcc1s
The up-regulation of neuronal glutaminase was demonstrated in situ in a murine model of HIV-1 encephalitis.
The memory deficits observed in nemy are because of reduced function of CytB561 (show CYB561 ELISA Kits) in specific brain regions that are involved in learning and memory.
the crystal structure of full-length KGA and present a small-angle X-ray scattering model for full-length GLS2 (show GLS2 ELISA Kits). These structures explain these proteins' compromised ability to assemble into catalytically active supra-tetrameric filaments, as previously shown for GAC.
GLS1 inhibition using BPTES reduced metabolic intermediates including thymidine and carbamoyl phosphate. Reduction of thymidine and carbamoyl-phosphate synthesis by BPTES treatment exacerbated pyrimidine supply by combination with 5-FU, which induced cell death synergistically in NSCLC
Glutaminase expression in tumor cells was significantly associated with a low level of tumor-infiltrating lymphocytesand poor disease-free survival in triple-negative breast cancers presenting with lymph node metastasis and high levels of tumor-infiltrating lymphocytes.
Study reports that GLS1 is a direct target of miR-23a in retinal pigment epithelium cells (RPE) providing evidence for a role in maintaining RPE cell function.
The relative expression of microRNA-153 and glutaminase in glioblastoma versus matched non-tumor tissues showed a reverse correlation, further indicating that microRNA-153 may negatively regulate glutaminase in vivo.
High GLS1 expression is associated with epithelial-mesenchymal transition in cancer.
Data suggest that glutaminase C (GAC) inhibition maybe a potential treatment strategy for acquired erlotinib-resistant non-small cell lung cancer (NSCLC).
Findings indicate a role for transcription factor c-Jun (show JUN ELISA Kits) as a driver of cancer cell metabolic reprogramming, and suggest that cancers overexpressing JUN (show JUN ELISA Kits) may be especially sensitive to glutaminase (GLS)-targeted therapies.
GLS1 was identified as a potential downstream target of the miR (show MLXIP ELISA Kits)-192/-204-HOTTIP axis in hepatocellular carcinoma.
This gene encodes the K-type mitochondrial glutaminase. The encoded protein is an phosphate-activated amidohydrolase that catalyzes the hydrolysis of glutamine to glutamate and ammonia. This protein is primarily expressed in the brain and kidney plays an essential role in generating energy for metabolism, synthesizing the brain neurotransmitter glutamate and maintaining acid-base balance in the kidney. Alternate splicing results in multiple transcript variants.
glutaminase kidney isoform, mitochondrial
, phosphate-activated glutaminase
, glutaminase C
, hypothetical protein
, L-glutamine amidohydrolase
, glutaminase, phosphate-activated
, glutaminase liver isoform, mitochondrial
, liver mitochondrial glutaminase