合成的[酪氨酸5,12，赖氨酸7] - 海胆精蛋白II肽（T22）与CD4细胞表面分子结合。
The synthetic [Tyr5,12,Lys7]-polyphemusin II peptide (T22) binds to the CD4 cell surface molecule.
作者信息
Weeks B S, Nomizu M, Otaka A, Weston C A, Okusu A, Tamamura H, Yamamoto N, Fujii N
机构信息
Department of Medicine, University of Pennsylvania, Philadelphia 19104, USA.
出版信息
Biochem Biophys Res Commun. 1995 Oct 13;215(2):626-31. doi: 10.1006/bbrc.1995.2510.
The [Tyr5,12,Lys7]-polyphemusin II peptide (T22) inhibits HIV-1 replication in lymphocytes. The mechanism of T22 inhibition of HIV-1 replication may involve T22 competition with HIV-1 for attachment sites on the plasma membrane of targeted cells. Here we find that the T22 peptide binds to the CD4 molecule in affinity columns. We also find that antiserum to CD4 inhibits cell attachment to T22. Further CD4+ transfected cells attach to T22 while their parental cells which do not express CD4 do not attach to T22. These data demonstrate that T22 binds to the CD4 molecule and supports the hypothesis that T22 inhibits HIV-1 replication by binding to the cell surface CD4 molecule and inhibiting uptake of the virus.
[酪氨酸5、12，赖氨酸7] - 多聚半胱氨酸II肽（T22）可抑制HIV-1在淋巴细胞中的复制。T22抑制HIV-1复制的机制可能涉及T22与HIV-1竞争靶细胞质膜上的附着位点。在此我们发现，T22肽在亲和柱中与CD4分子结合。我们还发现，抗CD4抗血清可抑制细胞与T22的附着。此外，转染了CD4的细胞可附着于T22，而其不表达CD4的亲代细胞则不附着于T22。这些数据表明，T22与CD4分子结合，并支持以下假说：T22通过结合细胞表面的CD4分子并抑制病毒摄取来抑制HIV-1复制。
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