Arg-Gly-Asp-Ser

91037-65-9

C15H27N7O8

DMSO : >= 55 mg/mL (126.90 mM); H2O : >= 25 mg/mL (57.68 mM)

Cytoskeleton

Arg-Gly-Asp-Ser is an integrin binding sequence that inhibits integrin receptor function, decreases systemic inflammation via inhibition of collagen-triggered activation of leukocytes and attenuates expression of inflammatory cytokines, iNOS and MMP-9. In Vitro: The Arg-Gly-Asp-Ser-modified surface causes up-regulation of alphavbeta3 integrin. Attachment to the Arg-Gly-Asp-Ser-treated membrane completely abolishes apoptosis induced by staurosporine, the Ca²⁺·Pi ion pair, and sodium nitroprusside. Arg-Gly-Asp-Ser-dependent resistance to apoptosis is eliminated, when the activity of the phosphatidylinositol 3-kinase pathway is inhibited^[1]. Arg-Gly-Asp-Ser interacts with survivin, as well as with procaspase-3, -8 and -9. Arg-Gly-Asp-Ser-peptide binding to survivin is found to be specific, at high affinity (K_d 27.5 uM) and locates at the survivin C-terminus. Arg-Gly-Asp-Ser-survivin interaction appears to play a key role, since Arg-Gly-Asp-Ser lost its anti-mitogenic effect in survivin-deprived cells with a specific siRNA^[4]. In Vivo: Arg-Gly-Asp-Ser (2.5 or 5 mg/kg, 1 h before LPS) significantly inhibits LPS-induced MMP-9 activity in BAL fluid 4 h post-LPS. Arg-Gly-Asp-Ser (1, 2.5 or 5 mg/kg, i.p.) administers 1 h before LPS inhibited LPS-induced increases in TNF-alpha and MIP-2 levels in BAL fluid at 4 h post-LPS^[2]. Arg-Gly-Asp-Ser peptide significantly reduces tumor necrosis factor (TNF)-alpha and macrophage inflammatory protein (MIP)-2 production, and decreases myeloperoxidase (MPO) and NF-kappaB activity^[3].