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Data show that 1,25-dihydroxyvitamin D (1,25D) downregulation of glutamine synthetase (GLUL (show GLUL Proteins); 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 (show GLUL Proteins) and SLC13A2 (show SLC13A2 Proteins)/FOXN1 (show FOXN1 Proteins)
GLUL (show GLUL Proteins) knockdown markedly inhibited the p38 MAPK (show MAPK14 Proteins) and ERK1 (show MAPK3 Proteins)/ERK2 (show MAPK1 Proteins) signaling pathways in cultured breast cancer cells and reduces their proliferation.
co-targeting glutamine synthetase (show GLUL Proteins) in stroma and glutaminase (show GLS Proteins) in cancer cells reduces tumor weight, nodules, and metastasis.
This study demonstrated that Influence of glutamine synthetase (show GLUL Proteins) 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 (show CRBN Proteins)) and degradation by the proteasome.
Studied molecular mechanisms of glutamine synthetase (show GLUL Proteins) mutations that lead to clinically relevant pathologies.
GLUL (show GLUL Proteins) rs10911021 is associated prospectively with adjudicated cardiovascular composite end points among overweight/obese individuals with type 2 diabetes.
Data show that glutamine synthetase (GS (show GLUL Proteins)) produces glutamine (show GFPT1 Proteins) (Gln) from tricarboxylic acid (TCA)-cycle-derived carbons.
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.
This study concludes that hepatic expression of alanine transaminase and glutathione synthetase (GS (show GSS Proteins)) are reduced in aged cows, and administration of 17beta-estradiol increases plasma estradiol and hepatic GS.
Data show that glutamine synthetase (GS (show GLUL Proteins))protein was preferentially expressed in hepatocytes adjacent to oxygen-supplying capillaries and in previously CPS-positive hepatocytes.
Diabetes induces TXNIP (show TXNIP Proteins) 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 (show GAL Proteins)-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 (show TYR Proteins) nitration.
modulation of intracellular glutamine levels by GS expression represents an endogenous mechanism through which mature adipocytes control the inflammatory response
GABABR2 (show GABBR2 Proteins) has a role as a regulator of glutamine synthetase (show GLUL Proteins) stability
the capacity for ammonia disposal correlated inversely with the expression of glutamine synthetase (show GLUL Proteins) in muscle
Glutamine synthetase (show GLUL Proteins) in astrocytes from entorhinal cortex of the triple transgenic animal model of Alzheimer's disease is not affected by pathological disease progression.
Renal glutamine synthetase (show GLUL Proteins) 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 (show GLUL Proteins) is required for the early steps of the cytokine response to endotoxins, and that its pharmacological inhibition may be exploited to treat inflammation.
BDNF (show BDNF Proteins) can up-regulate GLAST (show SLC1A3 Proteins) and GS and increase glutamate (show GRIN1 Proteins) uptake during hypoxia, and these functions may underlie its neuroprotective effects.
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)
, glutamate-ammonia ligase (glutamine synthetase)
, Glutamine synthetase (glutamate-ammonia ligase)
, glutamine synthetase 1