Mouse Gas1 Antibody

Gas1 (Growth Arrest Specific 1) is one of six structurally unrelated proteins that were identified by their increased expression in growth-arrested cells relative to actively proliferating cells (1, 2). Following mitogenic stimulation, Gas1 expression is transcriptionally suppressed by c-Myc as cells transit from G₀ to G₁ phases of the cell cycle (3, 4). Overexpression of Gas1 prevents S phase entry and DNA synthesis (5). Gas1-mediated blockade of the cell cycle is p53-dependent but does not require the transactivating domain of p53 (6). The mouse Gas1 cDNA encodes a 343 amino acid (aa) precursor that includes a 38 aa signal sequence, a 277 aa mature protein, and a 28 aa C-terminal propeptide. Gas1 contains Ala-rich and Asp-rich regions as well as an RGD sequence (5). Mature mouse and human Gas1 share 85% aa sequence identity. Mouse Gas1 is a 40 kDa GPI linked glycoprotein that is uniformly distributed on the cell surface (7). In contact inhibited vascular endothelial cells, Gas1 is induced by VE-Cadherin and VEGF expression and mediates the anti-apoptotic effect of VEGF (8). In contrast, Gas1 is induced in hippocampal neurons after NMDA exposure but functions as a pro-apoptotic effector of NMDA-mediated excitotoxicity (9). Gas1 exhibits a range of developmental effects including either promoting or inhibiting growth and differentiation of somite, limb, cerebellar, and eye tissues (10‑14). Gas1 mediates the antagonistic effect of Wnt proteins toward Shh function by binding the N-terminal region of Shh (11). The dependence of Gas1 functions on the cellular context has been addressed by suggesting that Gas1 could function as a co-receptor for GDNF family ligands (15). This speculation is supported by R&D Systems’ data that demonstrate direct binding of Gas1 to Artemin and Neurturin.