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一种与逆转录病毒包膜蛋白同源的合成肽可下调肿瘤坏死因子-α和干扰素-γ的mRNA表达。

A synthetic peptide homologous to retroviral envelope protein down-regulates TNF-alpha and IFN-gamma mRNA expression.

作者信息

Haraguchi S, Good R A, Cianciolo G J, Day N K

机构信息

Department of Pediatrics, All Children's Hospital, University of South Florida, St. Petersburg 33701.

出版信息

J Leukoc Biol. 1992 Oct;52(4):469-72. doi: 10.1002/jlb.52.4.469.

Abstract

We investigated the influence of CKS-17, a synthetic heptadecapeptide that corresponds to a highly conserved domain of the immunosuppressive retroviral envelope protein p15E, on staphylococcal enterotoxin B (SEB)-induced TNF-alpha gene expression in human peripheral blood mononuclear cells and highly purified human monocyte preparations, as well as the production of TNF-alpha protein, using human peripheral blood mononuclear cells. RNA hybridization studies show that CKS-17 inhibits SEB-induced TNF-alpha mRNA accumulation in human peripheral blood mononuclear cells and human monocytes. CKS-17 is also shown to be highly suppressive for SEB-induced production of TNF-alpha proteins. Similarly, CKS-17 inhibits expression of SEB-induced IFN-gamma mRNA in human peripheral blood mononuclear cells. These results suggest that CKS-17 down-regulates both TNF-alpha and IFN-gamma production at mRNA level.

摘要

我们研究了CKS - 17(一种合成的十七肽,对应于免疫抑制逆转录病毒包膜蛋白p15E的高度保守结构域)对人外周血单核细胞和高度纯化的人单核细胞制剂中葡萄球菌肠毒素B(SEB)诱导的肿瘤坏死因子-α(TNF-α)基因表达的影响,以及使用人外周血单核细胞对TNF-α蛋白产生的影响。RNA杂交研究表明,CKS - 17抑制人外周血单核细胞和人单核细胞中SEB诱导的TNF-α mRNA积累。CKS - 17还显示出对SEB诱导的TNF-α蛋白产生具有高度抑制作用。同样,CKS - 17抑制人外周血单核细胞中SEB诱导的干扰素-γ(IFN-γ)mRNA表达。这些结果表明,CKS - 17在mRNA水平下调TNF-α和IFN-γ的产生。

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