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http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3242| Title: | Type I phosphatidylinositol 4-phosphate 5-kinase controls neutrophil polarity and directional movement |
| Publisher: | Rockefeller University Press |
| Description: | Copyright by The Rockefeller University Press Directional cell movement in response to external chemical gradients requires establishment of front–rear asymmetry, which distinguishes an up-gradient protrusive leading edge, where Rac-induced F-actin polymerization takes place, and a down-gradient retractile tail (uropod in leukocytes), where RhoA-mediated actomyosin contraction occurs. The signals that govern this spatial and functional asymmetry are not entirely understood. We show that the human type I phosphatidylinositol 4-phosphate 5-kinase isoform β (PIPKIβ) has a role in organizing signaling at the cell rear. We found that PIPKIβ polarized at the uropod of neutrophil-differentiated HL60 cells. PIPKIβ localization was independent of its lipid kinase activity, but required the 83 C-terminal amino acids, which are not homologous to other PIPKI isoforms. The PIPKIβ C terminus interacted with EBP50 (4.1-ezrin-radixin-moesin (ERM)-binding phosphoprotein 50), which enabled further interactions with ERM proteins and the Rho-GDP dissociation inhibitor (RhoGDI). Knockdown of PIPKIβ with siRNA inhibited cell polarization and impaired cell directionality during dHL60 chemotaxis, suggesting a role for PIPKIβ in these processes. Peer reviewed |
| URI: | http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3242 |
| Other Identifiers: | The Journal of Cell Biology, Vol. 179, No. 7, pp. 1539-1553 0021-9525 http://hdl.handle.net/10261/3242 10.1083/jcb.200705044 |
| Appears in Collections: | Digital Csic |
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