Palumbo Roberta, De Marchis Francesco, Pusterla Tobias, Conti Antonio, Alessio Massimo, Bianchi Marco E
San Raffaele Research Institute, 20132 Milano, Italy.
J Leukoc Biol. 2009 Sep;86(3):617-23. doi: 10.1189/jlb.0908581. Epub 2009 Apr 28.
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-kappaB 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.
高迁移率族蛋白B1(HMGB1)是一种核蛋白,可作为组织损伤的信号,因为它由遭受创伤性死亡的细胞释放或由活化的天然免疫细胞分泌。细胞外HMGB1可引发多种细胞类型迁移至组织损伤部位,包括炎性细胞和干细胞。细胞外HMGB1激活的信号通路尚未完全明确:我们之前报道过细胞外信号调节激酶(ERK)和核因子κB(NF-κB)通路参与其中,我们在此报道Src也被激活。Src缺失或用激酶抑制剂PP2抑制可阻断向HMGB1的迁移。Src与黏着斑激酶(FAK)结合并介导其磷酸化以及黏着斑的形成。