• Purity

  >95%, by SDS-PAGE under reducing conditions and visualized by silver stain

• Endotoxin Level

  <0.10 EU per 1 μg of the protein by the LAL method.  

• Activity

  Measured by its binding ability in a functional ELISA. Immobilized rhGas1 at 1 μg/mL (100 μL/well) can bind rmArtemin at a linear range of 0.1-10 ng/mL.

• Source

  Mouse myeloma cell line, NS0-derived Leu40-Ser318, with a C-terminal 6-His tag

• Accession #

• N-terminal Sequence    
  Analysis

  Leu40

• Structure / Form

  Monomer

• Predicted Molecular Mass

  30.1 kDa

• SDS-PAGE

  40 kDa, reducing conditions

Background: Gas1

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 human Gas1 cDNA encodes a 345 amino acid (aa) precursor that includes a 39 aa signal sequence, a 279 aa mature protein, and a 27 aa C-terminal propeptide. Gas1 contains Ala-rich and Asp-rich regions as well as an RGD sequence (5). Mature human and mouse Gas1 share 85% aa sequence identity. Human 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 actions including either promoting or inhibiting growth and differentiation of somite, limb, cerebellar, and eye tissues (10 - 14). Gas1 contributes to the antagonistic effect of Wnt proteins toward Shh function by binding the N-terminal region of Shh (11). The dependence of Gas1 function 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 which demonstrate direct binding of Gas1 to Artemin and Neurturin.

• References:

1. Schneider, C. et al. (1988) Cell 54:787.

2. Mullor, J.L. and A.R. Altaba (2002) BioEssays 24:22.

3. Del Sal, G. et al. (1994) Proc. Natl. Acad. Sci. USA 91:1848.

4. Lee, T.C. et al. (1997) Proc. Natl. Acad. Sci. USA 94:12886.

5. Del Sal, G. et al. (1992) Cell 70:595.

6. Del Sal, G. et al. (1995) Mol. Cell. Biol. 15:7152.

7. Stebel, M. et al. (2000) FEBS Lett. 481:152.

8. Spagnuolo, R. et al. (2004) Blood 103:3005.

9. Mellstrom, B. et al. (2002) Mol. Cell Neurosci. 19:417.

10. Lee, K.K.H. et al. (2001) Dev. Biol. 234:188.

11. Lee, C.S. et al. (2001) Proc. Natl. Acad. Sci. USA 98:11347.

12. Liu, Y. et al. (2002) Development 129:5289.

13. Liu, Y. et al. (2001) Dev. Biol. 236:30.

14. Lee, C.S. et al. (2001) Dev. Biol. 236:17.

15. Schueler-Furman, O. et al. (2006) Trends Pharmacol. Sci. 27:72.

• Long Name:

  Growth-arrest-specific Protein 1

• Entrez Gene IDs:

  2619 (Human); 14451 (Mouse)

• Alternate Names:

  Gas1; GAS-1; growth arrest-specific 1; Growth arrest-specific gene-1; growth arrest-specific protein 1