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GLUL knockdown markedly inhibited the p38 MAPK (show MAPK14 ELISA Kits) and ERK1 (show MAPK3 ELISA Kits)/ERK2 (show MAPK1 ELISA Kits) signaling pathways in cultured breast cancer cells and reduces their proliferation.
co-targeting glutamine synthetase in stroma and glutaminase (show GLS ELISA Kits) 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 (show CRBN ELISA Kits)) 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 (show GFPT1 ELISA Kits) (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.
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 was highest in gluteus and semimembranous muscles and much lower in diaphragm and heart muscles.
Diabetes induces TXNIP (show TXNIP ELISA Kits) 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 ELISA Kits)-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 ELISA Kits) nitration.
modulation of intracellular glutamine levels by GS expression represents an endogenous mechanism through which mature adipocytes control the inflammatory response
GABABR2 (show GABBR2 ELISA Kits) 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.
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 (show BDNF ELISA Kits) can up-regulate GLAST (show SLC1A3 ELISA Kits) and GS and increase glutamate (show GRIN1 ELISA Kits) uptake during hypoxia, and these functions may underlie its neuroprotective effects.
This study concludes that hepatic expression of alanine transaminase and glutathione synthetase (GS (show GSS ELISA Kits)) 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)
, glutamine synthetase GlnA
, glutamate-ammonia ligase (glutamine synthetase)
, Glutamate-ammonia ligase
, cytoplasmic glutamine synthetase
, glutamine synthetase 2
, glutamine synthetase 1
, glutamine synthetase I
, mitochondrial glutamine synthetase
, glutamate-ammonia ligase
, glutamine synthetase type I
, glutamine synthetase type III
, Glutamine synthetase (glutamate-ammonia ligase)