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findings reveal that, in addition to the known formation of glutamine, the enzyme glutamine synthetase shows unknown activity in endothelial cell migration during pathological angiogenesis through RHOJ palmitoylation
In silico analysis potentially links GLUL SNPs with major depression disorder.
The SNP rs10911021 near glutamate-ammonia ligase is associated with oxidative stress in coronary heart disease patients from Pakistan.
ASCT2 was significantly overexpressed in the gastric cancer (GC) samples compared with adjacent non-cancerous gastric mucosa, in contrast, a significantly higher level of glutamine synthetase (GS) expression was observed in normal tissues than in GC samples compared with adjacent non-cancerous gastric mucosa.
The data identify GS activity as mediator of the proangiogenic, immunosuppressive, and pro-metastatic function of M2-like macrophages and highlight the possibility of targeting this enzyme in the treatment of cancer metastasis.
Data show that 1,25-dihydroxyvitamin D (1,25D) downregulation of glutamine synthetase (GLUL; GS)) was sufficient to reduce abundance and enzyme activity of GS.
genome-wide association study to identify genetic factors for familial hepatitis B virus-related hepatocellular carcinoma; results identified 2 large effect susceptible haplotypes located at GLUL and SLC13A2/FOXN1
GLUL knockdown markedly inhibited the p38 MAPK and ERK1/ERK2 signaling pathways in cultured breast cancer cells and reduces their proliferation.
co-targeting glutamine synthetase in stroma and glutaminase in cancer cells reduces tumor weight, nodules, and metastasis.
This study demonstrated that Influence of glutamine synthetase gene polymorphisms on the development of hyperammonemia during valproic acid-based therapy.
GS is acetylated at lysines 11 and 14, yielding a degron that is necessary and sufficient for binding and ubiquitylation by CRL4(CRBN) and degradation by the proteasome.
Studied molecular mechanisms of glutamine synthetase mutations that lead to clinically relevant pathologies.
GLUL rs10911021 is associated prospectively with adjudicated cardiovascular composite end points among overweight/obese individuals with type 2 diabetes.
Data show that glutamine synthetase (GS) produces glutamine (Gln) from tricarboxylic acid (TCA)-cycle-derived carbons.
findings point to SNP rs10911021 of GLULas an independent modulator of mortality in patients with type 2 diabetes
Data indicate that the triple stain of reticulin, glypican-3, and glutamine synthetae is useful in the differentiation of hepatocellular carcinoma, hepatic adenoma, and focal nodular hyperplasia.
Results highlight the diagnostic errors that can be caused by variant patterns of staining with glutamine synthetase and serum amyloid-associated protein in inflammatory hepatocellular adenoma and focal nodular hyperplasia.
High Glutamine synthetase expression is associated with epilepsy in newly diagnosed glioblastoma multiforme.
Glutamine synthetase expression is increased in regenerating hepatocytes and in early hepatocyte progenitor cells prior to morphological evidence of hepatocellular differentiation.
through a 3-stage genome-wide association study in 4188 type 2 diabetic patients, identified a novel susceptibility locus for coronary heart disease in the region of the GLUL gene
Glutamine synthetase expression was highest in gluteus and semimembranous muscles and much lower in diaphragm and heart muscles.
genetic deletion of Glul in endothelial cells impairs vessel sprouting during vascular development, whereas pharmacological blockade of glutamine synthetase suppresses angiogenesis in ocular and inflammatory skin disease while only minimally affecting healthy adult quiescent endothelial cells
Our study highlights a new role of GS in modulating immune response in microglia, providing insights into the pathogenic mechanisms associated with inflammation and new strategies of therapeutic intervention
We conclude that 1) GS-mediated ammonia recycling in the PT contributes to both basal and acidosis-stimulated ammonia metabolism and 2) adaptive changes in other proteins involved in ammonia metabolism occur in response to PT-GS-KO and cause an underestimation of the role of PT GS expression.
Diabetes induces TXNIP expressions at mRNA levels, but shows the opposite effect on GS.
Results indicate that astrocyte glutamine synthase may be the predominant contributor to the pathogenic mechanisms of D-gal-induced brain aging in mice.
Hepatic deletion of GS triggered systemic hyperammonemia, which was associated with cerebral oxidative stress as indicated by increased levels of oxidized RNA and enhanced protein Tyr nitration.
modulation of intracellular glutamine levels by GS expression represents an endogenous mechanism through which mature adipocytes control the inflammatory response
GABABR2 has a role as a regulator of glutamine synthetase stability
the capacity for ammonia disposal correlated inversely with the expression of glutamine synthetase in muscle
Glutamine synthetase in astrocytes from entorhinal cortex of the triple transgenic animal model of Alzheimer's disease is not affected by pathological disease progression.
In a transgenic mouse model of Alzheimer disease, found decrease in number of GS-positive astrocytes in prefrontal cortex from early to middle ages when compared with control animals.
Renal glutamine synthetase is expressed in type A intercalated cells, non-A, non-B intercalated cells, and distal convoluted tubule cells, but not in principal cells, type B intercalated cells, or connecting segment cells.
Methionine sulfoximine target glutamine synthetase is required for the early steps of the cytokine response to endotoxins, and that its pharmacological inhibition may be exploited to treat inflammation.
BDNF can up-regulate GLAST and GS and increase glutamate uptake during hypoxia, and these functions may underlie its neuroprotective effects.
Glutamine synthetase deficiency in murine astrocytes results in neonatal death.
Glutamine synthetase in muscle is required for glutamine production during fasting and extrahepatic ammonia detoxification
Reduction of GS in TGF-beta1-on-mice results from apoptosis of GS-positive hepatocytes rather than downregulation of GS expression
aspartate aminotransferase and glutamine synthetase have roles in glucocorticoid activation in mouse Schwann cells
There was a >100-fold difference in GS mRNA, protein, and enzyme-activity levels among organs, whereas there was only a 20-fold difference in the GS protein:mRNA ratio, suggesting extensive transcriptional and posttranscriptional regulation.
This study concludes that hepatic expression of alanine transaminase and glutathione synthetase (GS) are reduced in aged cows, and administration of 17beta-estradiol increases plasma estradiol and hepatic GS.
Data show that glutamine synthetase (GS)protein was preferentially expressed in hepatocytes adjacent to oxygen-supplying capillaries and in previously CPS-positive hepatocytes.
The protein encoded by this gene belongs to the glutamine synthetase family. It catalyzes the synthesis of glutamine from glutamate and ammonia. Glutamine is a main source of energy and is involved in cell proliferation, inhibition of apoptosis, and cell signaling. This gene is expressed during early fetal stages, and plays an important role in controlling body pH by removing ammonia from circulation. Mutations in this gene are associated with congenital glutamine deficiency. Several alternatively spliced transcript variants have been found for this gene.
cell proliferation-inducing protein 59
, glutamate decarboxylase
, glutamate--ammonia ligase
, glutamine synthase
, glutamine synthetase
, proliferation-inducing protein 43
, glutamate-ammonia ligase (glutamine synthase)
, glutamine synthetase (glnA)
, glutamate-ammonia ligase (glutamine synthetase)
, glutamate-ammonia ligase
, Glutamine synthetase (glutamate-ammonia ligase)
, glutamine synthetase 1
, Glutamate decarboxylase
, Glutamate--ammonia ligase
, glutamine synthetase 2