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Human Monoclonal GLUL Primary Antibody for ELISA, WB - ABIN561060
Herbert, Kuiperij, Verbeek: Optimisation of the quantification of glutamine synthetase and myelin basic protein in cerebrospinal fluid by a combined acidification and neutralisation protocol. in Journal of immunological methods 2012
Human Monoclonal GLUL Primary Antibody for FACS, IF - ABIN2722009
Shajahan-Haq, Cook, Schwartz-Roberts, Eltayeb, Demas, Warri, Facey, Hilakivi-Clarke, Clarke: MYC regulates the unfolded protein response and glucose and glutamine uptake in endocrine resistant breast cancer. in Molecular cancer 2014
ASCT2 (show SLC1A5 Antibodies) 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.
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 (show SLC13A2 Antibodies)/FOXN1 (show FOXN1 Antibodies)
GLUL knockdown markedly inhibited the p38 MAPK (show MAPK14 Antibodies) and ERK1 (show MAPK3 Antibodies)/ERK2 (show MAPK1 Antibodies) signaling pathways in cultured breast cancer cells and reduces their proliferation.
co-targeting glutamine synthetase in stroma and glutaminase (show GLS Antibodies) 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 Antibodies)) 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 Antibodies) (Gln) from tricarboxylic acid (TCA)-cycle-derived carbons.
Glutamine synthetase expression was highest in gluteus and semimembranous muscles and much lower in diaphragm and heart muscles.
Diabetes induces TXNIP (show TXNIP Antibodies) 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 Antibodies)-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 Antibodies) nitration.
modulation of intracellular glutamine (show GFPT1 Antibodies) levels by GS expression represents an endogenous mechanism through which mature adipocytes control the inflammatory response
GABABR2 (show GABBR2 Antibodies) 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 Antibodies) can up-regulate GLAST (show SLC1A3 Antibodies) and GS and increase glutamate (show GRIN1 Antibodies) 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 Antibodies)) 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