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用N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸激活巨噬细胞:蛋白激酶C和酪氨酸激酶的参与

Activation of macrophages with N-formyl-methionyl-leucyl-phenylalanine: involvement of protein kinase C and tyrosine kinase.

作者信息

Shrivastava Anju

机构信息

Department of Zoology, University of Delhi, Delhi 110 007, India.

出版信息

Indian J Exp Biol. 2007 Sep;45(9):755-63.

Abstract

N-formyl-methionyl-leucyl-phenylalanine (fMLP) a potent chemotactic peptide stimulates immune responses by activating macrophages and other cells of the immune system. The present study reports inhibition of fMLP-induced activation of murine peritoneal and P388D-1 macrophage cell line by protein kinase C (PKC) inhibitors, H-7 and chelerythrine chloride. Similarly, tumoricidal activity was also downregulated by protein tyrosine kinase (PTK) inhibitors genestein and lavendustin A. Further, fMLP increased tyrosine phosphorylation of several proteins in murine macrophages, which were inhibited in presence of genestein and lavendustin A. These findings suggest the involvement of PKC and PTK in the activation of murine macrophages with fMLP.

摘要

N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸(fMLP)是一种强效趋化肽,通过激活巨噬细胞和免疫系统的其他细胞来刺激免疫反应。本研究报告了蛋白激酶C(PKC)抑制剂H-7和氯化白屈菜红碱对fMLP诱导的小鼠腹腔巨噬细胞和P388D-1巨噬细胞系激活的抑制作用。同样,蛋白酪氨酸激酶(PTK)抑制剂染料木黄酮和薰衣草素A也下调了杀肿瘤活性。此外,fMLP增加了小鼠巨噬细胞中几种蛋白质的酪氨酸磷酸化,而在染料木黄酮和薰衣草素A存在的情况下这种磷酸化受到抑制。这些发现表明PKC和PTK参与了fMLP对小鼠巨噬细胞的激活过程。

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