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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Phosphatidylinositol 4-kinase, catalytic, alpha

phosphatidylinositol 4-kinase, PI4K230, PIK4CA
This gene encodes a phosphatidylinositol (PI) 4-kinase which catalyzes the first committed step in the biosynthesis of phosphatidylinositol 4,5-bisphosphate. The mammalian PI 4-kinases have been classified into two types, II and III, based on their molecular mass, and modulation by detergent and adenosine. The protein encoded by this gene is a type III enzyme that is not inhibited by adenosine. Two transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, ACID, HAD, Actin, V1a
Papers on phosphatidylinositol 4-kinase
A phosphoinositide conversion mechanism for exit from endosomes.
Haucke et al., Berlin, Germany. In Nature, Feb 2016
Removal of endosomal PI(3)P by MTM1 is accompanied by phosphatidylinositol 4-kinase-2α (PI4K2α)-dependent generation of PI(4)P and recruitment of the exocyst tethering complex to enable membrane fusion.
The leukodystrophy protein FAM126A (hyccin) regulates PtdIns(4)P synthesis at the plasma membrane.
De Camilli et al., New Haven, United States. In Nat Cell Biol, Jan 2016
FAM126A is an intrinsic component of the plasma membrane phosphatidylinositol 4-kinase complex that comprises PI4KIIIα and its adaptors TTC7 and EFR3 (refs ,).
Gene essentiality and synthetic lethality in haploid human cells.
Brummelkamp et al., Amsterdam, Netherlands. In Science, Dec 2015
This revealed a genetic cross-talk governing Golgi homeostasis, an additional subunit of the human oligosaccharyltransferase complex, and a phosphatidylinositol 4-kinase β adaptor hijacked by viruses.
GABARAP-mediated targeting of PI4K2A/PI4KIIα to autophagosomes regulates PtdIns4P-dependent autophagosome-lysosome fusion.
Yin et al., Dallas, United States. In Autophagy, Dec 2015
PI4K2A/PI4KIIα (phosphatidylinositol 4-kinase type 2 α), one of the 4 enzymes that catalyze PtdIns4P production in mammalian cells, promotes vesicle formation from the trans-Golgi network (TGN) and endosomes.
Currently recognized genes for schizophrenia: High-resolution chromosome ideogram representation.
Manzardo et al., Kansas City, United States. In Am J Med Genet B Neuropsychiatr Genet, Nov 2015
Recognized genes of clinical relevance, susceptibility or causation impact a broad range of biological pathways and mechanisms including ion channels (e.g., CACNA1B, CACNA1C, CACNA1H), metabolism (e.g., CYP1A2, CYP2C19, CYP2D6), multiple targets of neurotransmitter pathways impacting dopamine, GABA, glutamate, and serotonin function, brain development (e.g., NRG1, RELN), signaling peptides (e.g., PIK3CA, PIK4CA) and immune function (e.g., HLA-DRB1, HLA-DQA1) and interleukins (e.g., IL1A, IL10, IL6).
Modulation of the Host Lipid Landscape to Promote RNA Virus Replication: The Picornavirus Encephalomyocarditis Virus Converges on the Pathway Used by Hepatitis C Virus.
van Kuppeveld et al., Utrecht, Netherlands. In Plos Pathog, Sep 2015
Here we show that cardioviruses manipulate another PI4K, namely the ER-localized phosphatidylinositol 4-kinase III alpha (PI4KA), to generate PI4P-enriched ROs.
Bayesian phylogeny analysis of vertebrate serpins illustrates evolutionary conservation of the intron and indels based six groups classification system from lampreys for ∼500 MY.
Kumar, Kiel, Germany. In Peerj, 2014
Interestingly, the ancestral HCII/SERPIND1 locus (nested within PIK4CA) possesses group V4 serpin (A2APL1, homolog of α 2-AP/SERPINF2) of lampreys; hence, pointing to the fact that group V4 might have originated from group V2.
Multiple intestinal atresia with combined immune deficiency.
Notarangelo, Boston, United States. In Curr Opin Pediatr, 2014
Dysregulated RhoA signaling and defective expression of phosphatidylinositol 4-kinase IIIα represent biochemical cellular hallmarks of the disease.
Modeling the effects of cyclodextrin on intracellular membrane vesicles from Cos-7 cells prepared by sonication and carbonate treatment.
Waugh et al., London, United Kingdom. In Peerj, 2014
We treated these membranes, which mainly originate from the trans-Golgi network and endosomes, with cyclodextrin and measured the effects on their equilibrium buoyant density, protein content, represented by the palmitoylated protein phosphatidylinositol 4-kinase type IIα, and cholesterol.
Mammalian phosphatidylinositol 4-kinases as modulators of membrane trafficking and lipid signaling networks.
Waugh et al., London, United Kingdom. In Prog Lipid Res, 2013
Moreover, different permutations of phosphatidylinositol 4-kinase isozymes may be required for a single cellular function such as occurs during distinct stages of GPCR signalling and in Golgi to lysosome trafficking.
Phosphatidylinositol 4-kinases and PI4P metabolism in the nervous system: roles in psychiatric and neurological diseases.
Waugh et al., London, United Kingdom. In Mol Neurobiol, 2013
Recent work has shown that reduced expression of individual phosphatidylinositol 4-kinase isozymes is associated with impaired survival of specific neuronal populations within the CNS.
The role of phosphatidylinositol 4-kinases and phosphatidylinositol 4-phosphate during viral replication.
Neyts et al., Leuven, Belgium. In Biochem Pharmacol, 2013
It has been well documented that phosphatidylinositol 4-kinase IIIβ (PI4KIIIβ, EC is indispensable for viral RNA replication of several picornaviruses.
[Exploration for anti-enterovirus compounds and analysis on the mechanism of its inhibitory effect on virus infection].
Arita, Pedro II, Brazil. In Uirusu, 2012
Recently, PIK93, an inhibitor of host phosphatidylinositol 4-kinase III beta (PI4KB), was identified as a potent anti-enterovirus compound (Hsu et al., Cell 141:799-811).
Phosphatidylinositol 4-kinase IIα is palmitoylated by Golgi-localized palmitoyltransferases in cholesterol-dependent manner.
Yin et al., Dallas, United States. In J Biol Chem, 2012
Phosphatidylinositol 4-kinase IIalpha is palmitoylated by Golgi-localized palmitoyltransferases in cholesterol-dependent manner
Hepatitis C virus stimulates the phosphatidylinositol 4-kinase III alpha-dependent phosphatidylinositol 4-phosphate production that is essential for its replication.
Randall et al., Chicago, United States. In J Virol, 2011
These results suggest that hepatitis C virus NS5A modulation of PI4KA-dependent phosphatidylinositol 4-phosphate production influences replication complex formation.
Genetic and functional studies of phosphatidyl-inositol 4-kinase type IIIα.
Balla et al., Bethesda, United States. In Biochim Biophys Acta, 2011
confirmed the high copy number of PI4KIIIalpha transcript in K562 cells along with several genes located in the same region in Chr22, including two pseudogenes that cover most exons coding for isoform 1, consistent with chromosome amplification
Stabilization of phosphatidylinositol 4-kinase type IIbeta by interaction with Hsp90.
Albanesi et al., Dallas, United States. In J Biol Chem, 2011
Study identify the molecular chaperone Hsp90 as a binding partner of PI4KIIbeta, but not of PI4KIIalpha.
The role of the phosphatidylinositol 4-kinase PI4KA in hepatitis C virus-induced host membrane rearrangement.
Salloum et al., Ann Arbor, United States. In Plos One, 2010
PI4KA is necessary for the local enrichment of PI 4-phosphate at the hepatitis c virus membranous web.
Wnt3a-mediated formation of phosphatidylinositol 4,5-bisphosphate regulates LRP6 phosphorylation.
Wu et al., New Haven, United States. In Science, 2008
By screening a human kinase small interfering RNA library, we identified phosphatidylinositol 4-kinase type II alpha and phosphatidylinositol-4-phosphate 5-kinase type I (PIP5KI) as required for Wnt3a-induced LRP6 phosphorylation at Ser1490 in mammalian cells and confirmed that these kinases are important for Wnt signaling in Xenopus embryos.
Protein kinase D regulates vesicular transport by phosphorylating and activating phosphatidylinositol-4 kinase IIIbeta at the Golgi complex.
Pfizenmaier et al., Stuttgart, Germany. In Nat Cell Biol, 2005
We show that phosphatidylinositol 4-kinase IIIbeta (PI4KIIIbeta) - a key player in the structure and function of the Golgi complex - is a physiological substrate of PKD.
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