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Microarray analysis revealed that glutamate (Montrer GRIN2A Protéines) 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 (Montrer DCTN1 Protéines) levels in psychosis.
NQO1 (Montrer NQO1 Protéines) 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 (Montrer GABPA Protéines) 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 (Montrer HMOX1 Protéines)), and NADPH (Montrer NQO1 Protéines): quinone dehydrogenase-1 (NQO1 (Montrer NQO1 Protéines)...
Glutaminolysis is activated in ES2 (Montrer DGCR14 Protéines) and OVCAR3, though ES2 (Montrer DGCR14 Protéines) exclusively synthesizes amino acids and GSH. ES2 (Montrer DGCR14 Protéines) cells are more resistant to carboplatin than OVCAR3 and the abrogation of GSH production by BSO sensitizes ES2 (Montrer DGCR14 Protéines) to carboplatin. HNF1beta (Montrer HNF1B Protéines) regulates the expression of GCLC, but not GCLM (Montrer GCLM Protéines), and consequently GSH production in ES2 (Montrer DGCR14 Protéines)
miR-433 targets both catalytic (GCLc) and regulatory (GCLm) subunits of GCL.
Data suggest expression of hepatocyte GCLC and GCLM (Montrer GCLM Protéines) 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 (Montrer GCLM Protéines) expression.
Cigarette smoke-induced hypermethylation of the GCLC promoter is related to the initiation and progression of COPD (Montrer ARCN1 Protéines).
GCLC and GSS (Montrer GSS Protéines) 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 (Montrer IL1B Protéines) 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 (Montrer ROS1 Protéines)), 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 (Montrer THY1 Protéines)-cre mouse and at a later age by breeding with a CaMKII (Montrer CAMK2G Protéines)-ERT2 (Montrer MAPK3 Protéines)-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 (Montrer TGFB1 Protéines) suppresses GCLC and GCLM (Montrer GCLM Protéines) 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 (Montrer NFE2L2 Protéines), and its downstream antioxidant HO-1 (Montrer HMOX1 Protéines) and gamma-GCS (Montrer UGCG Protéines) in the glomeruli of diabetic mice
In first days of life luminescence measured was in all mice with distinct strain differences indicating NF-kappaB (Montrer NFKB1 Protéines), superoxide dismutase (Montrer SOD1 Protéines), 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 (Montrer GSS Protéines) (GS) (E.C. 188.8.131.52)
activation of GSK-3beta is a key mediator of the initial phase of acetaminophen-induced liver injury through modulating GCL and Mcl-1 (Montrer MCL1 Protéines) degradation, as well as JNK (Montrer MAPK8 Protéines) 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