syk-mediated translocation of pi3kδ to the leading edge controls lamellipodium formation and migration of leukocytessyk-mediated易位的pi3kδ前缘控制lamellipodium形成和白细胞的迁移.pdfVIP

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syk-mediated translocation of pi3kδ to the leading edge controls lamellipodium formation and migration of leukocytessyk-mediated易位的pi3kδ前缘控制lamellipodium形成和白细胞的迁移.pdf

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syk-mediated translocation of pi3kδ to the leading edge controls lamellipodium formation and migration of leukocytessyk-mediated易位的pi3kδ前缘控制lamellipodium形成和白细胞的迁移

Syk-Mediated Translocation of PI3Kd to the Leading Edge Controls Lamellipodium Formation and Migration of Leukocytes ¨ 1. 1. 2 1 ´ 3 4 2 Jurgen Schymeinsky , Cornelia Then , Anca Sindrilaru , Ronald Gerstl , Zoltan Jakus , Victor L. J. Tybulewicz , Karin Scharffetter-Kochanek , Barbara Walzog1* 1 Department of Physiology, Ludwig-Maximilians-University Munich, Munich, Germany, 2 Department of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany, 3 Department of Physiology, Semmelweis University School of Medicine, Budapest, Hungary, 4 Division of Immune Cell Biology, National Institute for Medical Research, London, United Kingdom The non-receptor tyrosine kinase Syk is mainly expressed in the hematopoietic system and plays an essential role in b2 integrin-mediated leukocyte activation. To elucidate the signaling pathway downstream of Syk during b2 integrin (CD11/ CD18)-mediated migration and extravasation of polymorphonuclear neutrophils (PMN), we generated neutrophil-like differentiated HL-60 (dHL-60) cells expressing a fluorescently tagged Syk mutant lacking the tyrosine residue at the position 323 (Syk-Tyr323) that is known to be required for the binding of the regulatory subunit p85 of the phosphatidylinositol 3-kinase (PI3K) class IA. Syk-Tyr323 was found to be critical for the enrichment of the catalytic subunit p110d of PI3K class IA as well as for the generation of PI3K products at the leading edge of the majority of polarized cells. In accordance, the translocation of PI3K p110d to the leading edge was diminished in Syk deficient murine PMN. Moreover, the expression of EGFP-Syk Y323F interfered with proper cell polarization and it imp