Src family kinases are necessary for cell migration induced by extracellular HMGB1

被引：49

作者：

Palumbo, Roberta ^{[1
]}

De Marchis, Francesco ^{[1
]}

Pusterla, Tobias ^{[1
,2
]}

Conti, Antonio ^{[1
]}

Alessio, Massimo ^{[1
]}

Bianchi, Marco E. ^{[2
]}

机构：

[1] San Raffaele Res Inst, I-20132 Milan, Italy

[2] San Raffaele Univ, Fac Med, Milan, Italy

来源：

JOURNAL OF LEUKOCYTE BIOLOGY | 2009年 / 86卷 / 03期

关键词：

chemokines; DAMP; danger signals; stem cells; tissue repair; GLYCATION END-PRODUCTS; FOCAL ADHESION KINASE; SMOOTH-MUSCLE-CELLS; INFLAMMATORY RESPONSES; SIGNAL-TRANSDUCTION; CYTOPLASMIC DOMAIN; NEURITE OUTGROWTH; TYROSINE KINASES; ACTIVATION; RECEPTOR;

D O I：

10.1189/jlb.0908581

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

HMGB1 is a nuclear protein that signals tissue damage, as it is released by cells dying traumatically or secreted by activated innate immunity cells. Extracellular HMGB1 elicits the migration to the site of tissue damage of several cell types, including inflammatory cells and stem cells. The identity of the signaling pathways activated by extracellular HMGB1 is not known completely: We reported previously that ERK and NF-kappa B pathways are involved, and we report here that Src is also activated. The ablation of Src or inhibition with the kinase inhibitor PP2 blocks migration toward HMGB1. Src associates to and mediates the phosphorylation of FAK and the formation of focal adhesions. J. Leukoc. Biol. 86: 617-623; 2009.

引用

页码：617 / 623

页数：7

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