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Arg-Gly-Asp-Ser

CAS No. : 91037-65-9

MCE 站：Arg-Gly-Asp-Ser

产品活性：Arg-Gly-Asp-Ser是整联蛋白结合序列，抑制整联蛋白受体功能，通过抑制胶原蛋白引发的白细胞活化减少全身炎症，并减弱炎性细胞因子，iNOS和MMP-9的表达。

研究领域：Cytoskeleton

作用靶点：Integrin

In Vitro: The Arg-Gly-Asp-Ser-modified surface causes up-regulation of αvβ3 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. 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 μM) 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.

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-α ａnd MIP-2 levels in BAL fluid at 4 h post-LPS. Arg-Gly-Asp-Ser peptide significantly reduces tumor necrosis factor (TNF)-α ａnd macrophage inflammatory protein (MIP)-2 production, ａnd decreases myeloperoxidase (MPO) ａnd NF-κB activity.

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