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α趋化因子,即基质细胞衍生因子-1α,与跨膜G蛋白偶联CXCR-4受体结合并激活多种信号转导途径。

The alpha-chemokine, stromal cell-derived factor-1alpha, binds to the transmembrane G-protein-coupled CXCR-4 receptor and activates multiple signal transduction pathways.

作者信息

Ganju R K, Brubaker S A, Meyer J, Dutt P, Yang Y, Qin S, Newman W, Groopman J E

机构信息

Divisions of Experimental Medicine, and Hematology/Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.

出版信息

J Biol Chem. 1998 Sep 4;273(36):23169-75. doi: 10.1074/jbc.273.36.23169.

Abstract

The alpha-chemokine stromal cell-derived factor (SDF)-1alpha binds to the seven transmembrane G-protein-coupled CXCR-4 receptor and acts to modulate cell migration and proliferation. The signaling pathways that mediate the effects of SDF-1alpha are not well characterized. We studied events following SDF-1alpha binding to CXCR-4 in a model murine pre-B cell line transfected with human CXCR-4. There was enhanced tyrosine phosphorylation and association of components of focal adhesion complexes such as the related adhesion focal tyrosine kinase, paxillin, and Crk. We also observed activation of phosphatidylinositol 3-kinase. Wortmannin, a selective inhibitor of phosphatidylinositol 3-kinase, partially inhibited the SDF-1alpha-induced migration and tyrosine phosphorylation of paxillin. SDF-1alpha treatment selectively activated p44/42 mitogen-activated protein kinase (Erk 1 and Erk 2) and its upstream kinase mitogen-activated protein kinase kinase but not p38 mitogen-activated protein kinase, c-Jun amino-terminal kinase or mitogen activated protein kinase kinase. We also observed that SDF-1alpha treatment increased NF-kappaB activity in nuclear extracts from the CXCR-4 transfectants. Taken together, these studies revealed that SDF-1alpha activates distinct signaling pathways that may mediate cell growth, migration, and transcriptional activation.

摘要

α-趋化因子基质细胞衍生因子(SDF)-1α与七次跨膜G蛋白偶联的CXCR-4受体结合,并调节细胞迁移和增殖。介导SDF-1α作用的信号通路尚未完全明确。我们在转染了人CXCR-4的小鼠前B细胞系模型中研究了SDF-1α与CXCR-4结合后的事件。发现酪氨酸磷酸化增强,并且粘着斑复合物的成分如相关粘着斑酪氨酸激酶、桩蛋白和Crk发生了结合。我们还观察到磷脂酰肌醇3激酶的激活。磷脂酰肌醇3激酶的选择性抑制剂渥曼青霉素部分抑制了SDF-1α诱导的迁移和桩蛋白的酪氨酸磷酸化。SDF-1α处理选择性地激活了p44/42丝裂原活化蛋白激酶(Erk 1和Erk 2)及其上游激酶丝裂原活化蛋白激酶激酶,但未激活p38丝裂原活化蛋白激酶、c-Jun氨基末端激酶或丝裂原活化蛋白激酶激酶。我们还观察到SDF-1α处理增加了CXCR-4转染细胞核提取物中的NF-κB活性。综上所述,这些研究表明SDF-1α激活了可能介导细胞生长、迁移和转录激活的不同信号通路。

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