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Data indicate that type I phosphatidylinositol 4-phosphate 5-kinase PIP5KIbeta mutants whose dimerization was impaired showed a severe decrease in PI(4,5)P2 production and plasma membrane delocalization.
Knockdown of PIP5K1B in fibroblasts reproduced abnormal actin cytoskeleton remodeling evidenced in Friedreich's ataxia patient cells.
Results identify PIPKIbeta as a novel regulator of focal adhesion disassembly and suggest that PIPKIbeta spatially regulates beta1 integrin endocytosis at adhesion sites to control cell migration.
Results identify an isoform-specific PDZ-binding motif in PIP5KIbeta, which confers specificity for PIP5KIbeta signaling at the uropod during leukocyte chemotaxis.
findings show that the human type I phosphatidylinositol 4-phosphate 5-kinase isoform beta (PIPKIbeta) has a role in organizing signaling at the cell rear
Syk-dependent phosphorylation of PIP5K1B is the dominant modification responsible for the decrease in cellular phosphatidylinositol 4,5-bisphosphate.
synthesis of PtdIns(4,5)P(2) mediated by PIP5KIbeta is rate limiting for apical but not basolateral endocytosis in polarized kidney cells
The results suggested that PIP5K1A and PIP5K1B may coordinately and/or redundantly function in the maintenance of sperm number and morphology during spermatogenesis.
Phosphatidylinositol 4-phosphate 5-kinase is essential for ROCK-mediated neurite remodeling
PIPKIalpha activity is involved in the actin remodeling that is a prerequisite for efficient phagocytosis
These results indicate that both Arf6 and PIP5K are involved in integrin-dependent bacterial uptake, and that Arf6 participates in both activation of PIP5K as well as in other events associated with bacterial uptake.
findings indicate that synthesis of phosphatidylinositol 4,5-bisphosphate (PIP2) by the three phosphatidylinositol 4-phosphate 5-kinase (PIP5K) isoforms Ialpha, Ibeta and Igamma is controlled by Rho GTPases
phosphatidylinositol phosphate kinase type I alpha is a negative regulator of FcepsilonRI-mediated cellular responses and anaphylaxis.
after stimulation of a G protein-coupled receptor, IP(3) is completely derived from a rapidly synthesized discrete pool of PIP(2) synthesized by PIP5KIalpha and PIP5KIbeta
Participates in the biosynthesis of phosphatidylinositol 4,5-bisphosphate. Mediates RAC1-dependent reorganization of actin filaments. Contributes to the activation of PLD2. Together with PIP5K1A is required after stimulation of G-protein coupled receptors for stable platelet adhesion (By similarity).
, phosphatidylinositol 4-phosphate 5-kinase type I beta
, phosphatidylinositol 4-phosphate 5-kinase type-1 beta
, phosphatidylinositol-4-phosphate 5-kinase type-1 beta
, protein STM-7
, ptdIns(4)P-5-kinase 1 beta
, type I phosphatidylinositol 4-phosphate 5-kinase beta
, type I phosphatidylinositol-4-phosphate 5-kinase beta
, phosphatidylinositol 4-phosphate 5-kinase type I alpha
, phosphatidylinositol-4-phosphate 5-kinase type I alpha
, phosphatidylinositol-4-phosphate 5-kinase type I beta
, phosphatidylinositol-4-phosphate 5-kinase, type 1 alpha
, phosphatidylinositol-4-phosphate 5-kinase, type 1, beta
, ptdIns(4)P-5-kinase beta
, phosphatidylinositol-4-phosphate 5-kinase, type I, beta
, phosphatidylinositol-4-phosphate 5-kinase type-1 beta-like