Mouse Gas1 (Growth arrest-specific protein 1) ELISA Kit (E-EL-M3134)

This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Mouse Gas1. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Mouse Gas1 and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Mouse Gas1, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The OD value is proportional to the concentration of Mouse Gas1. You can calculate the concentration of Gas1 in the samples by comparing the OD of the samples to the standard curve.

Growth Arrest Specific 1 (Gas1) is highly expressed in growth-arrested cells. c-Myc transcriptionally represses Gas1 during G0-to-G1 cell cycle transition, and Gas1 overexpression blocks S-phase entry and DNA synthesis in a p53-dependent manner independent of p53’s transactivating domain. Murine Gas1 is a 40 kDa cell surface GPI-anchored glycoprotein. Its 343-amino-acid precursor contains a signal peptide, a mature domain with Ala-rich, Asp-rich and RGD motifs, and a C-terminal propeptide; mature mouse and human Gas1 share 85% sequence identity. Gas1 exhibits context-dependent activities. It confers VEGF-mediated anti-apoptosis in vascular endothelial cells but promotes NMDA-induced neuronal excitotoxic apoptosis. It modulates the growth and differentiation of somite, limb, cerebellar and eye tissues. As a key SHH coreceptor, Gas1 binds lipid-modified ShhN by recognizing its palmitate and cholesterol moieties and interacts with 20(S)-hydroxycholesterol. It transfers ShhN to PTCH1/PTCH2 to activate smoothened signaling, reversing early reports of its inhibitory role in this pathway. Gas1 also antagonizes Shh signaling via N-terminal Shh binding and serves as a potential coreceptor for GDNF family ligands including Artemin and Neurturin.