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High GLS1 expression is associated with autosomal-dominant polycystic kidney disease.
Glutaminase plays an important role in cancerous cells metabolism and Helicobacter pylori. The expression of the enzyme is lower in patients with Helicobacter pylori infection
HSF1 stimulated GLS1-dependent mTOR activation to promote colorectal carcinogenesis.
GLS1 is highly expressed in hepatocellular carcinoma (HCC), and correlates with poor prognosis. GLS1 is exclusively expressed in the mitochondrial matrix. Upregulation of GLS1 is positively associated with advanced clinicopathological features and stemness phenotype. GLS1 regulates stemness properties via ROS/Wnt/beta-catenin signaling and that GLS1 knockout inhibits tumorigenicity in vivo.
We report an inborn error of metabolism caused by an expansion of a GCA-repeat tract in the 5' untranslated region of the gene encoding glutaminase (GLS) that was identified through detailed clinical and biochemical phenotyping, combined with whole-genome sequencing.
Data suggest that GAC exhibits allosteric inhibition by compounds/ligands (antineoplastic agents) that bind competitively with glutamine.
Overexpressing glutaminase abolished the inhibitory effects of miR-1-3p on bladder cancer cell proliferation, migration, and invasion and glutaminase depletion resulted in the prolonged expression of gammaH2AX, an established biomarker for DNA damage.
These results reveal that GAC is post-translationally regulated by phosphorylation, which affects cellular glutamine metabolism and glutaminase-related cell phenotype.
In silico analysis potentially links GLS SNPs with Alzheimer disease and type 2 diabetes.
Del11q-positive CLL lymphocytes exhibit altered glutamine metabolism and differential response to GLS1 and glucose metabolism inhibition.
Overexpression of miR-513c suppresses neuroblastoma cells' migration, invasion, and proliferation. We demonstrate the glutaminase (GLS) is a direct target of miR-513c in human neuroblastoma cells.
the present findings enriched our knowledge by demonstrating a significant association of PKM2 and GLS1 with oxaliplatin-resistance in CRC.
miR-137 was decreased in melanoma tissue, and the low miR-137 levels and high glutaminase expression are independent risk factors in melanoma. miR-137 suppressed the proliferation and glutamine catabolism of melanoma cells.
Gls is a novel ERRalpha target gene.
ZIC5 positively regulated the proliferation, migration (Fig. 2), and survival (Fig. 5) of PCa and CRC cells
the crystal structure of full-length KGA and present a small-angle X-ray scattering model for full-length GLS2. 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
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.
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.
results show that GLS1 mutant mice display moderate impairments of hippocampal glutamatergic neurotransmission and moderate changes in adaptive behaviors that have been shown to participate to the development of depressive-like state.
Findings provide the first evidence that glutaminase C overexpression in the brain has deleterious effects on learning and synaptic integrity in vivo.
Our results suggested that glutamine metabolism is involved in the pathogenesis of rheumatoid arthritis and that GLS1 plays an important role in regulating rheumatoid arthritis fibroblast-like synoviocyte proliferation
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(PAG) is mainly active in mouse kidney, brain and liver, and shows different kinetics depending on which type of PAG 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.
identified a novel distant regulatory element located approximately 120kb downstream of the gls promoter, and examined its regulatory relevance to gls gene expression in C2C12 cells
In wild-type (WT) mice, GLS1 gene expression was highest in the hippocampus and cortex, where it was reduced by about 50% in Glutaminase-deficient mice.
These results show that necrotic neurons activate in microglia a MyD88-dependent pathway responsible for a pro-inflammatory response that also leads to increased neurotoxic activity through induction of glutaminase.
GLS1 heterozygous (GLS1 het) mice showed about a 50% global reduction in glutaminase activity and showed hippocampal hypometabolism mainly in the CA1 subregion and subiculum.
The memory deficits observed in nemy are because of reduced function of CytB561 in specific brain regions that are involved in learning and memory.
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.
, L-glutamine amidohydrolase
, glutaminase kidney isoform, mitochondrial
, glutaminase C
, phosphate-activated glutaminase
, glutaminase, phosphate-activated