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

Jana Barlic; Joseph D. Andrews; Alyson A. Kelvin; Steven E. Bosinger; Mark E. DeVries; Luoling Xu; Tomas Dobransky; Ross D. Feldman; Stephen S.G. Ferguson; David J. Kelvin

doi:10.1038/79767

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

Jana Barlic, Joseph D. Andrews, Alyson A. Kelvin, Steven E. Bosinger, Mark E. DeVries, Luoling Xu, Tomas Dobransky, Ross D. Feldman, Stephen S.G. Ferguson, David J. Kelvin

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202 Citas (Scopus)

Resumen

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 β-arrestin complexes with Hck or c-Fgr. Formation of β-arrestin-Hck complexes led to Hck activation and trafficking of the complexes to granule-rich regions. Granulocytes expressing a dominant-negative β-arrestin-mutant did not release granules or activate tyrosine kinases after IL-8 stimulation. Thus, β-arrestins regulate chemokine-induced granule exocytosis, indicating a broader role for β-arrestins in the regulation of cellular functions than was previously suspected.

Idioma original	English
Páginas (desde-hasta)	227-233
Número de páginas	7
Publicación	Nature Immunology
Volumen	1
N.º	3
DOI	https://doi.org/10.1038/79767
Estado	Published - sep. 2000
Publicado de forma externa	Sí

ASJC Scopus Subject Areas

Immunology and Allergy
Immunology

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title = "Regulation of tyrosine kinase activation and granule release through β-arrestin by CXCRI",

abstract = "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 β-arrestin complexes with Hck or c-Fgr. Formation of β-arrestin-Hck complexes led to Hck activation and trafficking of the complexes to granule-rich regions. Granulocytes expressing a dominant-negative β-arrestin-mutant did not release granules or activate tyrosine kinases after IL-8 stimulation. Thus, β-arrestins regulate chemokine-induced granule exocytosis, indicating a broader role for β-arrestins in the regulation of cellular functions than was previously suspected.",

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AU - Barlic, Jana

AU - Andrews, Joseph D.

AU - Kelvin, Alyson A.

AU - Bosinger, Steven E.

AU - DeVries, Mark E.

AU - Xu, Luoling

AU - Dobransky, Tomas

AU - Feldman, Ross D.

AU - Ferguson, Stephen S.G.

AU - Kelvin, David J.

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AB - 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 β-arrestin complexes with Hck or c-Fgr. Formation of β-arrestin-Hck complexes led to Hck activation and trafficking of the complexes to granule-rich regions. Granulocytes expressing a dominant-negative β-arrestin-mutant did not release granules or activate tyrosine kinases after IL-8 stimulation. Thus, β-arrestins regulate chemokine-induced granule exocytosis, indicating a broader role for β-arrestins in the regulation of cellular functions than was previously suspected.

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

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