CST, 33381T, GCLM (F7J2D) Rabbit Monoclonal Antibody

Monoclonal Antibody for studying GCLM. Validated for Western Blotting,Immunoprecipitation,Immunofluorescence (Frozen). Available in 2 sizes. Highly specific and rigorously validated in-house, GCLM (F7J2D) Rabbit Monoclonal Antibody (CST #33381) is ready to ship. Product Usage Information Western Blotting: 1:1000 Immunoprecipitation: 1:100 Immunofluorescence (Frozen): 1:200 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting, Immunoprecipitation, Immunofluorescence (Frozen) Specificity / Sensitivity GCLM (F7J2D) Rabbit Monoclonal Antibody recognizes endogenous levels of total GCLM protein. Species reactivity by immunofluorescence is mouse only. Species Reactivity: Human, Mouse, Rat Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu212 of human GCLM protein. Background Glutamate-cysteine ligase modifier subunit (GCLM) is a component of the heterodimeric enzyme glutamate-cysteine ligase (GCL), which catalyzes the rate-limiting step in glutathione (GSH) biosynthesis, a ubiquitous intracellular peptide that plays vital roles in antioxidant defense, detoxification, cell proliferation, and other cellular functions (1,2). is one of a set of inhibitory ferroptosis genes that are normally repressed by the transcription factor BACH1 (a regulator in heme and iron metabolism) but are coordinately upregulated upon induction of ferroptosis with erastin (3). Additionally, when cells are starved for cysteine, the non-canonical activity of GCL can catalyze the synthesis of γ-glutamyl-peptide, therefore maintaining glutamate homeostasis to protect cells against ferroptosis (4). GCLM overexpression in bladder cancer is correlated with immune filtration and poor prognosis, and knockdown of GCLM can significantly suppress the colony formation ability of tumor cells, thus suggesting that GCLM is a potential therapeutic target (5). Indeed, treatment of BLCA cells with MTX-211, an EFGR and PI3K kinase inhibitor, promoted NFR2 degradation and subsequent downregulation of GCLM expression, resulting in decreased GSH levels and cell proliferation inhibition (6). Polymorphisms in the 5′ promoter region of are also associated with an increased risk of myocardial infarction (7), and GCLM may be implicated in other diseases where oxidative stress plays a significant role. Alternate Names Gamma-ECS regulatory subunit; Gamma-glutamylcysteine synthetase regulatory subunit; GCLM; GCS light chain; GLCLR; Glutamate--cysteine ligase modifier subunit; Glutamate--cysteine ligase regulatory subunit; glutamate-cysteine ligase (gamma-glutamylcysteine synthetase), regulatory (30.8kD); glutamate-cysteine ligase modifier subunit; glutamate-cysteine ligase modifier subunit delta2 alternative splicing; glutamate-cysteine ligase regulatory protein; glutamate-cysteine ligase, modifier subunit; GSC light chain; GSH0 Specification REACTIVITY: H M R SENSITIVITY: Endogenous MW (kDa): 28 Source/Isotype: Rabbit IgG