CST, 47342T, GNAS/G alpha-s (E4G1G) Rabbit Monoclonal Antibody

Monoclonal Antibody for studying GNAS. Validated for Western Blotting. Available in 2 sizes. Highly specific and rigorously validated in-house, GNAS/G alpha-s (E4G1G) Rabbit Monoclonal Antibody (CST #47342) is ready to ship. Product Usage Information Western Blotting: 1:1000 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 Specificity / Sensitivity GNAS/G alpha-s (E4G1G) Rabbit Monoclonal Antibody recognizes endogenous levels of total GNAS/Gαs protein. Species Reactivity: Human, Mouse, Rat Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human GNAS/Gαs protein. Background G protein-coupled receptors (GPCRs) transmit extracellular signals through heterotrimeric G proteins (guanine nucleotide-binding proteins) (1). G proteins have three main subunits: Gα, Gβ, and Gγ. In the quiescent state, the GDP bound Gα is associated with Gβγ. Binding of ligands to GPCR causes the exchange of GDP for GTP on Gα, leading to its dissociation from the Gβγ complex (2). The released GTP-Gα further activates downstream effectors to initiate signaling events. G-protein-mediated signaling is terminated by hydrolysis of GTP by Gα intrinsic GTP hydrolase and reassociation of Gα with Gβγ to form the inactive heterotrimer. There are four subclasses of Gα protein, Gαs, Gαi/o, Gαq/11, and Gα12/13 (3), and each is linked to a unique signaling pathway. Gαs is encoded by the gene. This G protein subunit is associated with a wide spectrum of disorders (4). The GTP bound Gαs activates adenylyl cyclase, which catalyzes the conversion of ATP into the second messenger cAMP and initiates the downstream PKA pathway (5). Mutations on residue Arg201 or Gln227 result in loss of GTP hydrolase activity (6), leading to constitutive activation of Gαs, which contributes to tumor progression (7,8), fibrous dysplasia of bone (9), and McCune-Albright syndrome, a disorder that causes abnormal skin pigmentation, scar tissue formation on bone, and growth-regulating gland malfunction (10). Heterozygous loss-of-function mutations in Gαs lead to Albright hereditary osteodystrophy (AHO), a disease characterized by short stature, obesity, brachydactyly, subcutaneous ossification, and dental deficits (11). Alternate Names Adenylate cyclase-stimulating G alpha protein; AHO; alternative gene product encoded by XL-exon; C20orf45; extra large alphas protein; G protein subunit alpha S; G-alpha(s); GNAS; GNAS complex locus; GNAS1; GNAS2; GPSA; GSA; GSP; guanine nucleotide binding protein (G protein), alpha stimulating activity polypeptide 1; guanine nucleotide regulatory protein; Guanine nucleotide-binding protein G(s) subunit alpha isoforms short; guanine nucleotide-binding protein G(s) subunit alpha isoforms XLas; MGC33735; NESP; PHP1A; PHP1B; PHP1C; PITA3; POH; protein ALEX; protein GNAS; protein SCG6 (secretogranin VI); SCG6; secretogranin VI; SgVI Specification REACTIVITY: H M R SENSITIVITY: Endogenous MW (kDa): 42, 45 Source/Isotype: Rabbit IgG