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Microarray analysis revealed that glutamate (show GRIN2A ELISA Kits) cysteine ligasec overexpression and thus enhanced glutathione production has a broad impact on gene expression that largely affects different processes in young and old flies.
investigation of mutations in GCL modifier subunit and the GCL catalytic subunit that modify catalytic activity and lower glutathione levels
Neuronal overexpression of GCLc in a long-lived background extended mean and maximum life spans up to 50%, without affecting the rate of oxygen consumption by the flies
The reversibility of the dephosphorylation-dependent activation was indicated by the time-dependent inactivation of the in vitro activated Drosophila GCL, by preincubation with MgATP.
that the longevity effects of GCLc are dependent on dosage and that there are specific tissues (mushroom bodies, motor neurons, and transverse muscle cells) particularly sensitive to the benefits of GCLc overexpression.
GSH biosynthesis in the nucleus is associated with migration of only the GCLc subunit from the cytoplasm into the nucleus, and this migration requires the presence of an intact nuclear localization signal
GCLC polymorphisms correlated with brain GSH and Glu (show DCTN1 ELISA Kits) levels in psychosis.
NQO1 (show NQO1 ELISA Kits) and GCLC were both functionally sufficient to autonomously confer a tamoxifen-resistant metabolic phenotype, characterized by i) increased mitochondrial biogenesis, ii) increased ATP production and iii) reduced glutathione levels.
(i) melatonin counteracted UVR-induced alterations in the ATP synthesis and reduced free radical formation; (ii) melatonin induced the translocation of Nrf2 (show GABPA ELISA Kits) transcription factor from the cytosol into the nucleus resulting in, (iii) melatonin enhanced gene expression of phase-2 antioxidative enzymes including gamma-glutamylcysteine synthetase (gamma-GCS), heme oxygenase-1 (HO-1 (show HMOX1 ELISA Kits)), and NADPH (show NQO1 ELISA Kits): quinone dehydrogenase-1 (NQO1 (show NQO1 ELISA Kits)...
Glutaminolysis is activated in ES2 (show DGCR14 ELISA Kits) and OVCAR3, though ES2 (show DGCR14 ELISA Kits) exclusively synthesizes amino acids and GSH. ES2 (show DGCR14 ELISA Kits) cells are more resistant to carboplatin than OVCAR3 and the abrogation of GSH production by BSO sensitizes ES2 (show DGCR14 ELISA Kits) to carboplatin. HNF1beta (show HNF1B ELISA Kits) regulates the expression of GCLC, but not GCLM (show GCLM ELISA Kits), and consequently GSH production in ES2 (show DGCR14 ELISA Kits)
miR-433 targets both catalytic (GCLc) and regulatory (GCLm) subunits of GCL.
Data suggest expression of hepatocyte GCLC and GCLM (show GCLM ELISA Kits) can be regulated by dietary component; alpha-lipoic acid, a vitamin B complex nutrient, protects against oxidative stress/cytotoxicity induced by cadmium via restoration of GCLC and GCLM (show GCLM ELISA Kits) expression.
Cigarette smoke-induced hypermethylation of the GCLC promoter is related to the initiation and progression of COPD (show ARCN1 ELISA Kits).
GCLC and GSS (show GSS ELISA Kits) were expressed at higher levels in colon cancer tissue, as compared with normal mucosa.
The Kaplan-Meier analysis shows that rs3736729 on GCLC presents a significant association with disease-free survival and overall survival.
H2S upregulates GCLC and GSH and inhibits IL-1beta (show IL1B ELISA Kits) levels, which may be what mediates the beneficial effects of H2S-rich compounds in mitigating the pathogenesis of metabolic syndrome and atherosclerosis
Data show that the catalytic subunit of glutamate cysteine ligase (Gclc)-derived glutathione buffers reactive oxygen species (ROS (show ROS1 ELISA Kits)), and regulates metabolic reprogramming.
To study the biological effects of low GSH levels, we disrupted its synthesis both at birth by breeding a Gclc loxP mouse with a thy1 (show THY1 ELISA Kits)-cre mouse and at a later age by breeding with a CaMKII (show CAMK2G ELISA Kits)-ERT2 (show MAPK3 ELISA Kits)-Cre (FIGSKO mouse). FIGSKO mice also develop cognitive abnormalities, i.e. learning impairment and nesting behaviors based on passive avoidance, T-Maze, and nesting behavior tests
A floxed Gclc mouse was generated and crossed with a transgenic mouse expressing Cre in the lens to generate the Lens Glutathione Synthesis Knockout mouse in which de novo GSH synthesis was completely abolished in the lens.
Clinically relevant levels of TGF-beta1 (show TGFB1 ELISA Kits) suppresses GCLC and GCLM (show GCLM ELISA Kits) expression in mouse lung.
Data show for the first time that GCLC may serve a dual role, as a surrogate marker for cellular redox state as well as malignant potential of melanoma cells.
The impacts of four clinical missense mutations on GCLC enzymatic function in vivo and in vitro, was evaluated.
tBHQ has beneficial effects on reducing hyperglycemia-induced kidney injury, which is associated with the enhanced expression of Nrf2 (show NFE2L2 ELISA Kits), and its downstream antioxidant HO-1 (show HMOX1 ELISA Kits) and gamma-GCS (show UGCG ELISA Kits) in the glomeruli of diabetic mice
In first days of life luminescence measured was in all mice with distinct strain differences indicating NF-kappaB (show NFKB1 ELISA Kits), superoxide dismutase (show SOD1 ELISA Kits), gamma-glutamylcysteine synthetase, and antioxidant responsive element activity.
Hypoxia decreased 2 key enzyme activities that regulate GSH synthesis, glutamate cysteine ligase (GCL) (E.C. 126.96.36.199) and glutathione synthase (show GSS ELISA Kits) (GS) (E.C. 188.8.131.52)
activation of GSK-3beta (show GSK3b ELISA Kits) is a key mediator of the initial phase of acetaminophen-induced liver injury through modulating GCL and Mcl-1 (show MCL1 ELISA Kits) degradation, as well as JNK (show MAPK8 ELISA Kits) activation in liver
Glutamate-cysteine ligase, also known as gamma-glutamylcysteine synthetase is the first rate-limiting enzyme of glutathione synthesis. The enzyme consists of two subunits, a heavy catalytic subunit and a light regulatory subunit. This locus encodes the catalytic subunit, while the regulatory subunit is derived from a different gene located on chromosome 1p22-p21. Mutations at this locus have been associated with hemolytic anemia due to deficiency of gamma-glutamylcysteine synthetase and susceptibility to myocardial infarction.
glutamate--cysteine ligase catalytic subunit
, glutamate-cysteine ligase, catalytic subunit
, gamma-Glutamylcysteine synthetase
, gamma-Glutamylcysteine synthetase catalytic subunit
, gamma-glutamylcysteine ligase
, glutamate cysteine ligase
, glutamate-cysteine ligase
, gamma glutamylcysteine synthetase
, glutamate--cysteine ligase, chloroplastic
, GCS heavy chain
, gamma-glutamylcysteine synthetase
, gamma GCS-HS
, gamma-glutamylcysteine synthetase heavy subunit
, Glutamylcysteine gamma synthetase light chain
, glutamate-cysteine ligase catalytic subunit