anti-Glutamate-Cysteine Ligase, Catalytic Subunit (GCLC) 抗体产品概述

Fruit Fly (Drosophila melanogaster) Glutamate-Cysteine Ligase, Catalytic Subunit (GCLC) interaction partners

1. we report phenotypic analysis of a complete loss-of-function mutant in the gamma-glutamylcysteine synthetase catalytic subunit (Gclc) gene in the fruit fly Drosophila melanogaster.Gclc encodes the evolutionarily conserved catalytic component of the enzyme that conjugates glutamate and cysteine in the GSH biosynthesis pathway.

2. Microarray analysis revealed that glutamate 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.

3. investigation of mutations in GCL modifier subunit and the GCL catalytic subunit that modify catalytic activity and lower glutathione levels

4. 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

5. 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.

6. 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.

7. 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

Human Glutamate-Cysteine Ligase, Catalytic Subunit (GCLC) interaction partners

1. Study found that the frequency of C/T polymorphism genotype of GCLC gene in patients with pulmonary tuberculosis is 36.4%.

2. the present study demonstrated that cells transformed by chronic exposure to 3MC exhibited inhibition of GSH biosynthesis by suppression of GCL protein expression and reduction of cysteine availability, which may subsequently render cells vulnerable to oxidative stress.

3. Glutathione biosynthesis during the lipopolysaccharide-induced inflammatory response in THP-1 macrophages is tightly and differentially regulated via GCLC and GCLM subunits of glutamate cysteine ligase.

4. High expression of GCLC in tumor tissue may be a potential predictor of treatment failure.

5. gamma-GCS has a role in chemo- and radio-resistance of human hepatocellular carcinoma cells

6. The findings indicate that expression of the transcription factor NRF2 and its effector GCL are both profoundly deregulated in endometriotic lesions towards increased growth and fibrogenetic processes.

7. Taken together, our findings provide evidence that G9a protects head and neck squamous cell carcinomas (HNSCC)cells against chemotherapy by increasing the synthesis of GSH, and imply G9a as a promising target for overcoming cisplatin resistance in HNSCC

8. A panel consisting of IGFBP1, KIM1, GCLC and GSTM1 genes could be used in combination for early screening of CKDu, whereas these genes in addition with FN1, IGFBP3 and KLK1 could be used to monitor progression of CKDu. The regulation of these genes has to be studied on larger populations to validate their efficiency for further clinical use.

9. High GCLC expression is associated with chemotherapy resistance in breast cancer.

10. Knockdown of CD44 reduced the protein level of xCT, a cystine transporter, and increased oxidative stress. However, an increase in GSH was also observed and was associated with enhanced chemoresistance in CD44-knockdown cells. Increased GSH was mediated by the Nrf2/AP-1-induced upregulation of GCLC, a subunit of the enzyme catalyzing GSH synthesis

11. GCLC polymorphisms correlated with brain GSH and Glu levels in psychosis.

12. NQO1 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.

13. (i) melatonin counteracted UVR-induced alterations in the ATP synthesis and reduced free radical formation; (ii) melatonin induced the translocation of Nrf2 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), and NADPH: quinone dehydrogenase-1 (NQO1...

14. Glutaminolysis is activated in ES2 and OVCAR3, though ES2 exclusively synthesizes amino acids and GSH. ES2 cells are more resistant to carboplatin than OVCAR3 and the abrogation of GSH production by BSO sensitizes ES2 to carboplatin. HNF1beta regulates the expression of GCLC, but not GCLM, and consequently GSH production in ES2

15. miR-433 targets both catalytic (GCLc) and regulatory (GCLm) subunits of GCL.

16. Data suggest expression of hepatocyte GCLC and GCLM 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 expression.

17. Cigarette smoke-induced hypermethylation of the GCLC promoter is related to the initiation and progression of COPD.

18. GCLC and GSS were expressed at higher levels in colon cancer tissue, as compared with normal mucosa.

19. The Kaplan-Meier analysis shows that rs3736729 on GCLC presents a significant association with disease-free survival and overall survival.

20. H2S upregulates GCLC and GSH and inhibits IL-1beta levels, which may be what mediates the beneficial effects of H2S-rich compounds in mitigating the pathogenesis of metabolic syndrome and atherosclerosis

Mouse (Murine) Glutamate-Cysteine Ligase, Catalytic Subunit (GCLC) interaction partners

1. The findings indicate that expression of the transcription factor NRF2 and its effector GCL are both profoundly deregulated in endometriotic lesions towards increased growth and fibrogenetic processes.

2. Retinal GCLC was significantly increased in rd10 mice at P21 as well as GSSG. Our results suggest alterations in retinal GCLC content and GSH and/or its precursors in these two RP animal models. Regulation of the enzymes related to GSH metabolism and the retinal concentration of glutamate may be a possible target to delay especially cone death in Retinitis Pigmentosa

3. Data show that the catalytic subunit of glutamate cysteine ligase (Gclc)-derived glutathione buffers reactive oxygen species (ROS), and regulates metabolic reprogramming.

4. 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-cre mouse and at a later age by breeding with a CaMKII-ERT2-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

5. 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.

6. Clinically relevant levels of TGF-beta1 suppresses GCLC and GCLM expression in mouse lung.

7. 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.

8. The impacts of four clinical missense mutations on GCLC enzymatic function in vivo and in vitro, was evaluated.

9. tBHQ has beneficial effects on reducing hyperglycemia-induced kidney injury, which is associated with the enhanced expression of Nrf2, and its downstream antioxidant HO-1 and gamma-GCS in the glomeruli of diabetic mice

10. In first days of life luminescence measured was in all mice with distinct strain differences indicating NF-kappaB, superoxide dismutase, gamma-glutamylcysteine synthetase, and antioxidant responsive element activity.

11. Hypoxia decreased 2 key enzyme activities that regulate GSH synthesis, glutamate cysteine ligase (GCL) (E.C. 6.3.2.2) and glutathione synthase (GS) (E.C. 6.3.2.3)

12. activation of GSK-3beta is a key mediator of the initial phase of acetaminophen-induced liver injury through modulating GCL and Mcl-1 degradation, as well as JNK activation in liver

13. These findings demonstrate that TAT-mediated transduction of wild-type or dominant-inhibitory mutants of the Glutamate cysteine ligase (GCL) subunits is a viable means of manipulating cellular GCL activity.

14. The GCLc protein was widely expressed throughout the embryo, and, in general, it co-localized with the Gclc mRNA.

15. study demonstrates that platelet-derived growth factor increases transcription of the gamma-glutamylcysteine synthetase heavy subunit in NIH 3T3 fibroblasts via H2O2 and activation of protein kinase C

16. The Gclc, the gene that encodes the catalytic subunit of the enzyme glutamate cysteine ligase, was used as a molecular surrogate for investigating the mechanisms by which TGF-beta suppressed Phase II gene expression.

17. Results of this study suggest that mechanisms of modulation of eukaryotic GCL enzymes may include specific binding of ligands such as pyridine dinucleotide phosphates and reversible protein phosphorylation.

18. Results suggest that TNF-alpha elevates the expression of lens epithelium-derived growth factor (LEDGF) and that LEDGF is one of the transactivators of gamma-glutamylcysteine synthetase heavy subunit gene.

19. glutamate-cysteine ligase activity is an important factor in determining acetaminophen-induced liver injury in C57Bl/6 male mice

20. These results suggest that intense noise exposure facilitates the expression of GCL catalytic subunit in the cochlea possibly through the activation of transcription factors including AP-1 and NF-kappaB.