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Phosphatidylinositol-4-phosphate 5-kinase, type I, gamma

PIP5KIgamma, type I PIP kinase, PIP5KC
This locus encodes a type I phosphatidylinositol 4-phosphate 5-kinase. The encoded protein catalyzes phosphorylation of phosphatidylinositol 4-phosphate, producing phosphatidylinositol 4,5-bisphosphate. This enzyme is found at synapses and has been found to play roles in endocytosis and cell migration. Mutations at this locus have been associated with lethal congenital contractural syndrome. Alternatively spliced transcript variants encoding different isoforms have been described.[provided by RefSeq, Sep 2010] (from NCBI)
Top mentioned proteins: Actin, gelsolin, PIP5KIalpha, Rhodopsin, RhoA
Papers on PIP5KIgamma
NMDA receptor-mediated PIP5K activation to produce PI(4,5)P₂ is essential for AMPA receptor endocytosis during LTD.
GeneRIF
Kanaho et al., Tsukuba, Japan. In Neuron, 2012
NMDA receptor activation controls AMPA AMPA AMPA receptor endocytosis during hippocampal LTD by regulating PIP5Kgamma661 activity at postsynapses.
An association between type Iγ PI4P 5-kinase and Exo70 directs E-cadherin clustering and epithelial polarization.
GeneRIF
Ling et al., Rochester, United States. In Mol Biol Cell, 2012
PIPKIgamma and phosphatidyl inositol phosphate pools at nascent E-cadherin contacts cue Exo70 targeting and orient the tethering of exocyst-associated E-cadherin
EZH2 regulates neuronal differentiation of mesenchymal stem cells through PIP5K1C-dependent calcium signaling.
GeneRIF
Hung et al., Taiwan. In J Biol Chem, 2011
EZH2 regulates neuronal differentiation of mesenchymal stem cells through PIP5K1C-dependent calcium signaling.
PIPKIγ regulates β-catenin transcriptional activity downstream of growth factor receptor signaling.
GeneRIF
Anderson et al., Madison, United States. In Cancer Res, 2011
A novel mechanism in which PIPKIgamma expression and catalytic activity enhance beta-catenin nuclear translocation and expression of its target genes to promote tumorigenic phenotypes.
PIPKIγ regulates focal adhesion dynamics and colon cancer cell invasion.
GeneRIF
Huang et al., Lexington, United States. In Plos One, 2010
PIPKIgamma positively regulates focal adhesion dynamics and cancer invasion, most probably through PIP-mediated vinculin activation.
Regulation of insulin secretion by phosphatidylinositol-4,5-bisphosphate.
Halban et al., Genève, Switzerland. In Traffic, 2010
Blocking PIP(2) with PH-PLC-GFP or PIP5KIgamma RNAi did not impact on glucose-stimulated secretion although susceptibility to apoptosis was increased.
Comparative analysis of normal versus CLL B-lymphocytes reveals patient-specific variability in signaling mechanisms controlling LFA-1 activation by chemokines.
Laudanna et al., Verona, Italy. In Cancer Res, 2010
Finally, phosphatidylinositol-4-phosphate 5-kinase isoform 1gamma (PIP5KC) was found without any regulatory role in all patients.
FAK, PIP5KIgamma and gelsolin cooperatively mediate force-induced expression of alpha-smooth muscle actin.
McCulloch et al., Toronto, Canada. In J Cell Sci, 2009
Type-I phosphatidylinositol 4-phosphate 5 kinase-gamma (PIP5KIgamma), which generates PtdIns(4,5)P(2), associated with FAK and was required for force-mediated SMA-promoter activity and actin assembly.
Regulation of conformer-specific activation of the integrin LFA-1 by a chemokine-triggered Rho signaling module.
Impact
Laudanna et al., Verona, Italy. In Nat Immunol, 2009
The Rho effectors PLD1 and PIP5KC were also critical to LFA-1 affinity modulation.
Loss of PIP5KIbeta demonstrates that PIP5KI isoform-specific PIP2 synthesis is required for IP3 formation.
Abrams et al., Philadelphia, United States. In Proc Natl Acad Sci U S A, 2008
We have also observed that platelets lacking both PIP5KIalpha and PIP5KIbeta have a complete loss of thrombin-induced IP(3) synthesis even though they still contain PIP5KIgamma, the predominant PIP5KI isoform in platelets.
Loss of PIP5KIgamma, unlike other PIP5KI isoforms, impairs the integrity of the membrane cytoskeleton in murine megakaryocytes.
GeneRIF
Abrams et al., Philadelphia, United States. In J Clin Invest, 2008
These findings demonstrate a unique role for PIP5KIgamma in the anchoring of the cell membrane to the cytoskeleton in megakaryocytes, probably through a pathway involving talin.
Phosphatidylinositol-4,5 bisphosphate produced by PIP5KIgamma regulates gelsolin, actin assembly, and adhesion strength of N-cadherin junctions.
GeneRIF
McCulloch et al., Toronto, Canada. In Mol Biol Cell, 2007
PIP5KIgamma-mediated generation of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) at sites of N-cadherin contacts regulates intercellular adhesion strength, an effect due in part to PI(4,5)P2-mediated regulation of gelsolin.
PIP5KI gamma is required for cardiovascular and neuronal development.
GeneRIF
Abrams et al., Philadelphia, United States. In Proc Natl Acad Sci U S A, 2007
Type I phosphatidylinositol-4-phosphate 5-kinase (PIP5KI) isoforms have overlapping, but not completely redundant, functions within cells; targeted disruption of PIP5KIgamma causes widespread developmental and cellular defects.
Beyond the epithelium: cadherin function in fibrous connective tissues.
Review
McCulloch et al., Toronto, Canada. In Febs Lett, 2007
Work over the last several years has documented an expanding list of molecules which function to regulate N-cadherin mediated junctions such as: Fer, PTP1B, cortactin, calcium, gelsolin, PIP5KIgamma, PIP2, and the Rho family of GTPases.
ARF6 regulates a plasma membrane pool of phosphatidylinositol(4,5)bisphosphate required for regulated exocytosis.
Martin et al., Madison, United States. In J Cell Biol, 2003
That the depletion of PIP2 and PIP5K from the plasma membrane caused the inhibition of DCV exocytosis was demonstrated directly in permeable cell reconstitution studies in which overexpression or addition of PIP5KIgamma restored Ca2+-dependent exocytosis.
Phosphatidylinositol phosphate 5-kinase Ibeta recruits AP-2 to the plasma membrane and regulates rates of constitutive endocytosis.
Roth et al., Dallas, United States. In J Cell Biol, 2003
When expression of PIP5KIbeta was inhibited with small interference RNA in HeLa cells, expression of PIP5KIalpha was also reduced slightly, but PIP5KIgamma expression was increased.
Dynamin at actin tails.
De Camilli et al., New Haven, United States. In Proc Natl Acad Sci U S A, 2002
Here we show that endogenous dynamin 2, as well as green fluorescence protein fusion proteins of both dynamin 1 and 2, is present in actin comets generated by Listeria or by type I PIP kinase (PIPK) overexpression.
Type I phosphatidylinositol 4-phosphate 5-kinase isoforms are specifically stimulated by phosphatidic acid.
Anderson et al., Madison, United States. In J Biol Chem, 1994
Based on functional studies, the 68-kDa protein is indistinguishable from the type I PIP kinase previously characterized from human erythrocyte membranes (Bazenet, C. E., Ruano, A.R., Brockman, J.L., and Anderson, R.A. (1990) J. Biol.
The human erythrocyte contains two forms of phosphatidylinositol-4-phosphate 5-kinase which are differentially active toward membranes.
Anderson et al., Madison, United States. In J Biol Chem, 1990
Fractionation of the membrane-bound PIP kinase activities by phosphocellulose separated activity into two peaks, which eluted at 0.6 M NaCl (type I PIP kinase) and 1.0 M NaCl (type II PIP kinase).
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