Ask about this productRelated genes to: GCLC Blocking Peptide
- Gene:
- GCLC NIH gene
- Name:
- glutamate-cysteine ligase catalytic subunit
- Previous symbol:
- GLCLC, GLCL
- Synonyms:
- GCS
- Chromosome:
- 6p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-24
- Date modifiied:
- 2019-04-23
Related products to: GCLC Blocking Peptide
Related articles to: GCLC Blocking Peptide
- Adolescent idiopathic scoliosis (AIS) involves systemic bone-metabolic dysregulation and paraspinal microenvironment remodeling, but whether nutrition-related micronutrient-associated molecular programs overlap with these alterations remains unclear. Vitamin E (VE), comprising lipid-soluble tocopherols and tocotrienols, is linked to membrane protection, lipid peroxidation control, inflammatory mediator regulation, and endothelial responses. This study examined whether VE-related molecular signatures converge on AIS-associated redox, lipid-inflammatory, vascular, and multicellular remodeling programs. Peripheral blood miRNA data (GSE235203) and bone marrow transcriptomic data (GSE110359) were integrated using HERB-based compound mapping, VE-AIS shared-target enrichment, feature prioritization, intradisease GSEA, single-cell localization, CellChat analysis, and NHANES contextualization. HERB mapping generated a VE/tocopherol-related prioritization signal, not direct evidence of VE involvement in AIS. Forty-two shared VE-AIS targets were enriched mainly in oxidative stress, glutathione/peroxidase activity, and glutathione metabolism, with additional lipid-inflammatory and vascular signals. Five prioritized genes (SOD1, GCLC, PTGS1, PTGS2, and KDR) defined redox-buffering, lipid-inflammatory, and vascular-response axes. Single-cell and CellChat analyses localized these signatures mainly to endothelial, dendritic/APC-like, MSC-like, and stromal/osteogenic populations, suggesting a predicted concave-side enrichment of inflammatory-endothelial-stromal communication. Structural analyses supported the computational plausibility of α-tocopherol compatibility with selected proteins, particularly PTGS2. No AIS cohort with measured VE exposure or status was analyzed. NHANES provided external clinical nutrition context rather than AIS-specific validation. Overall, VE-related signatures overlapped with redox, lipid-inflammatory, vascular-response, and multicellular remodeling programs in AIS. These findings generate testable molecular hypotheses but do not show that VE intake, tocopherol status, or supplementation modifies AIS risk, severity, or progression. - Source: PubMed
Publication date: 2026/08/06
Ma YingHan YuankunGeng ZhizhongFang SitongRen JunWang ShoujianHe TianxiangKong LingjunFang Min - Early embryonic development depends on precise redox homeostasis and mitochondrial quality control; however, how AMPK regulates embryonic fate through mitophagy remains unclear. In this study, integrated transcriptomic and proteomic analyses of Tibetan sheep embryos from the morula to blastocyst stages identified a GSH-AMPK-PINK1/PARKIN-mediated mitophagy axis as a key pathway governing mitochondrial homeostasis. Subsequently, functional validation was performed using in vitro embryo culture models with either GSH synthesis inhibition or AMPK inhibition. Under GSH synthesis inhibition, endogenous antioxidant capacity was markedly impaired, as evidenced by a 53% reduction in GCLC expression, while GPX4 expression showed no significant change. The energy-sensing molecules AMPK and phosphorylated AMPK (p-AMPK) were downregulated by 71.32% and 46.38%, respectively, accompanied by decreased expression of PINK1 (66.5%) and PARKIN (29.2%), consistent with multi-omics enrichment results. Mitochondrial functional assays revealed elevated mitochondrial membrane potential, increased MitoSOX fluorescence, reduced mitochondria-lysosome colocalization, and decreased LC3-positive puncta, indicating pronounced suppression of selective mitophagy. To further verify the central regulatory role of AMPK, an AMPK inhibition model was established. AMPK suppression did not significantly alter GSH levels but reproduced mitochondrial dysfunction and mitophagy defects highly similar to those observed under GSH synthesis inhibition, demonstrating that AMPK serves as a critical signaling hub linking redox imbalance to mitochondrial quality control. Collectively, this study systematically elucidates a causal cascade-GSH depletion→AMPK inactivation→inhibition of PINK1/PARKIN-mediated mitophagy→mitochondrial dysfunction→impaired embryonic development-and provides robust multi-omics and functional evidence for a redox-energy regulatory mechanism essential for early embryonic development. - Source: PubMed
Publication date: 2026/08/03
Li TianhaoBai XuefengLiao YuejiaoZuo QiyongLiu XinCui YanYu SijiuPan Yangyang - : Dihydromyricetin (DHM) is a food-derived flavonoid enriched in vine tea and has been reported to possess antioxidant and metabolism-regulating properties. This study was designed to characterize the multi-level nutritional responses to dietary DHM supplementation, with emphasis on hepatic redox-inflammatory status, jejunal barrier-related phenotypes, cecal microbiota remodeling, hepatic metabolomic alterations, and homocysteine (Hcy) metabolism-related markers in mice. : Forty-eight healthy mice were assigned to a basal-diet control group or diets containing 50, 100, or 200 mg/kg DHM for 4 weeks. Growth performance, serum biochemistry, antioxidant parameters, hepatic antioxidant-related expression, hepatic inflammatory cytokines, jejunal morphology and tight junction proteins, cecal 16S rRNA profiles, hepatic metabolomics, and Hcy metabolism-related markers were assessed. : Dietary DHM improved serum and hepatic antioxidant status, as reflected by increased T-AOC and GSH-Px activity and decreased MDA concentrations ( < 0.05). DHM also modulated the hepatic cytokine profile, with decreased TNF-α concentration ( < 0.05) and increased IL-10 concentration ( < 0.01). DHM increased hepatic Nrf2 protein abundance, HO-1 protein abundance, and Gclc mRNA expression ( < 0.05). DHM also improved jejunal villus architecture, as indicated by increased villus height, decreased crypt depth, and an increased villus height-to-crypt depth ratio ( < 0.05). Jejunal Occludin and ZO-1 protein expression were increased in the DHM-treated groups ( < 0.05). Cecal microbiota analysis showed increased richness and diversity indices and altered microbial community structure. Hepatic metabolomics revealed changes involving vitamin B6 metabolism, purine metabolism, the pentose phosphate pathway, and α-linolenic acid metabolism. Serum Hcy levels decreased ( < 0.05), accompanied by increased hepatic BHMT and MTHFR protein abundance ( < 0.01). : Dietary DHM supplementation improved hepatic redox status and supported a less pro-inflammatory cytokine profile in mice, accompanied by enhanced jejunal barrier-related phenotypes, cecal microbiota remodeling, hepatic metabolic alterations, and Hcy metabolism-related responses. These findings provide a multi-level nutritional evaluation of DHM and suggest its potential relevance for supporting intestinal barrier integrity and hepatic metabolic homeostasis under basal physiological conditions. - Source: PubMed
Publication date: 2026/07/22
Liang WenjiaoTang LishiyuanFan JinghuiHuang RuiChen JiaxuanQian Lichun - MASLD is a disorder linked to lipid metabolism and obesity, increasingly prevalent among sedentary people and leading to hepatic fibrosis. Cyclodipeptides (CDPs) have promising anti-obesogenic and liver-protective potential. CDP treatment was evaluated in a chronic MASLD model using female Wistar rats fed an obesogenic diet, with assessments of insulin resistance, glucose tolerance, liver damage, oxidative stress, and the expression of genes related to metabolic function. MASLD CDP-treated rats showed low visceral adipose tissue (VAT) content, improved insulin responsiveness and glucose tolerance, reduced steatosis, and reversed oxidant stress and the , , and expression. Furthermore, MASLD-related dysregulation of genes involved in lipid metabolism was restored, including vLDL transport (, , and ), β-oxidation (, , and ), lipogenesis ( and ), and fatty acid transport ( and ). In accordance, genes of key signaling pathways were also restored, including , , and , along with fibrosis and inflammation , , , and . In VAT of MASLD animals, crown-like structures and adiposity density were diminished by CDP treatment, with increased expression of genes associated with beige-like adipose tissue remodeling, including , , , , , , , and . Consistently, the UCP1 and PGC-1α protein expression was increased in the VAT of MASLD animals treated with CDPs. The anti-MASLD effects of CDPs were associated with reversal of key pathogenic markers in the liver and VAT, suggesting remodeling of white adipose tissue (WAT) toward a beige-like adipose tissue phenotype. The findings suggest that CDPs may modulate adipose tissue structure and adipogenesis, underscoring their therapeutic relevance for MASLD. - Source: PubMed
Publication date: 2026/07/15
Figueroa-Guzmán CitlaliCampos-Morales Marlene EstefaníaMartínez-Alcantar LorenaHernández-Padilla LauraSánchez-Duarte ElizabethSánchez-Briones Luis AlbertoLópez-Bucio Jesús SalvadorCampos-García Jesús - The gastrointestinal epithelium forms a critical barrier that regulates nutrient absorption while preventing the translocation of harmful luminal contents. Disruption of this barrier initiates a coordinated wound healing response involving epithelial restitution, proliferation, and differentiation. Focal adhesion kinase (FAK) is central to this process, regulating focal adhesion (FA) turnover and cytoskeletal dynamics required for epithelial migration. Activation of FAK via phosphorylation at tyrosine 397 (Y397) promotes cell motility, proliferation, and survival, whereas loss of function impairs mucosal repair and exacerbates tissue injury. Effective wound healing also requires tight regulation of reactive oxygen species (ROS). The nuclear factor erythroid 2-related factor 2 (NRF2) pathway governs antioxidant defenses by inducing cytoprotective genes, including SOD1, CAT, GCLC, GCLM, and NQO1, restoring redox homeostasis and limiting inflammation. NRF2 deficiency results in increased oxidative stress, heightened inflammatory signaling, and delayed wound healing. While both FAK and NRF2 are independently essential for gastrointestinal wound healing, their mechanistic relationship remains unclear. Emerging evidence suggests that they may be functionally linked through redox-dependent signaling where FAK-mediated ROS production may promote NRF2 activation, while NRF2-driven antioxidant responses maintain conditions necessary for sustained FAK signaling. This coordinated interaction highlights a redox-sensitive feedback mechanism critical for efficient gastrointestinal wound repair. - Source: PubMed
Publication date: 2026/07/16
Cleveland Olivia GVomhof-DeKrey Emilie E