Regulation of tyrosine kinase activation and granule release through β-arrestin by CXCRI

被引：182

作者：

Barlic, J

Andrews, JD

Kelvin, AA

Bosinger, SE

DeVries, ME

Xu, LL

Dobransky, T

Feldman, RD

Ferguson, SSG

Kelvin, DJ

机构：

[1] John P Robarts Res Inst, Lab Mol Immunol & Inflammat, London, ON N6G 2V4, Canada

[2] Univ Western Ontario, Dept Microbiol & Immunol, London, ON N6A 5C1, Canada

[3] John P Robarts Res Inst, Neurodegenerat Dis Grp, London, ON N6G 5K8, Canada

[4] Univ Western Ontario, Dept Med, London, ON N6A 5K8, Canada

[5] Univ Western Ontario, Dept Physiol, London, ON N6A 5K8, Canada

[6] Univ Western Ontario, Dept Pharmacol, London, ON N6A 5K8, Canada

[7] Univ Western Ontario, Dept Toxicol, London, ON N6A 5K8, Canada

[8] John P Robarts Res Inst, London, ON N6A 5K8, Canada

来源：

NATURE IMMUNOLOGY | 2000年 / 1卷 / 03期

关键词：

D O I：

10.1038/79767

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Chemoattractant-stimulated granule release from neutrophils, basophils and eosinophils is critical for the innate immune response against infectious bacteria. Interleukin 8 (IL-8) activation of the chemokine receptor CXCRI was found to stimulate rapid formation of beta-arrestin complexes with Hck or c-Fgr, Formation of beta-arrestin-Hck complexes led to Hck activation and trafficking of the complexes to granule-rich regions. Granulocytes expressing a dominant-negative beta-arrestin-mutant did not release granules or activate tyrosine kinases after IL-8 stimulation. Thus, beta-arrestins regulate chemokine-induced granule exocytosis, indicating a broader role for beta-arrestins in the regulation of cellular functions than was previously suspected.

引用

页码：227 / 233

页数：7

共 47 条

[1] β-Arrestins regulate interleukin-8-induced CXCR1 internalization [J].