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anti-Human PIP5K1A Anticorps:
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Human Polyclonal PIP5K1A Primary Antibody pour ELISA, WB - ABIN544190
Loijens, Anderson: Type I phosphatidylinositol-4-phosphate 5-kinases are distinct members of this novel lipid kinase family. dans The Journal of biological chemistry 1997
Show all 3 Pubmed References
The results suggest that PIP5KA is a novel degradative substrate of NEDD4 and that the PIP5KA-dependent phosphatidylinositol 4,5-diphosphate pool contributing to breast cancer cell proliferation through PI3K/Akt activation is negatively controlled by NEDD4.
PIP5K1alpha was associated with poor patient outcome in triple-negative BC. It increased expression of pSer-473 AKT and invasiveness of triple-negative MDA-MB-231 cells. Inhibition reduced expression of pSer-473 AKT and its downstream effectors in xenograft tumors. In ER(+) cancer cells, PIP5K1alpha acted on pSer-473 AKT, and was in complexes with VEGFR2, serving as co-factor of ER-alpha to regulate activities of targe...
KRAS-specific interactor that mediates oncogenic KRAS signaling and proliferation
Blockade of IQGAP1 interaction with PIPKIalpha or PI(3)K inhibited PtdIns(3,4,5)P3 generation and signalling, and selectively diminished cancer cell survival.
These results indicate that PP1 is recruited to the extracellular calcium-dependent E-cadherin-catenin-PIP5K1a complex in the plasma membrane to activate PIP5K1a, which is required for PLC-g1 activation leading to keratinocyte differentiation.
PIP5K1A modulates ribosomal RNA gene silencing through its interaction with histone H3 lysine 9 trimethylation and heterochromatin protein HP1-alpha.
PIP5K1A is modified by polySUMO-2 only during apoptosis.
CD28 regulates phosphatidylinositol 4,5-biphosphate turnover by recruiting and activating phosphatidylinositol 4-phosphate 5-kinases alpha in human primary CD4(+) T lymphocytes.
Results define the role of PIPKI-alpha in cell migration and describes a new mechanism for the spatial regulation of Rac1 activity that is critical for cell migration.
Localized production of Phosphatidylinositol 4,5-bisphosphate by PIP5K1A is required for invadopodia formation by breast cancer cells.
Membrane ruffling requires coordination between this enzyme and Rac signaling.
in addition to its effects upon Rac activity, Ajuba can also influence cell migration through regulation of PI(4,5)P2 synthesis through direct activation of PIPKIalpha enzyme activity
identified apoptotic stimuli that initiate a signaling pathway during cell death that leads to caspase-independent downregulation of PIP5Kalpha.
Type I phosphatidylinositol-4-phosphate-5-kinase (PI5KI) alpha and gamma isoforms were identified as the enzymes responsible for PIP2 synthesis in natural killer cells.
beta-arrestins direct the localization of PIP5K Ialpha and PIP(2) production to agonist-activated 7TMRs, thereby regulating receptor internalization
PI4P5-K Ialpha-mediated PIP(2) production is crucial for HIV-1 entry and the early steps of infection in permissive lymphocytes.
Extracellular calcium (Cao) stimulated PIP5K1alpha recruitment to the E-cadherin-catenin complex in the plasma membrane.
The data suggest that activation of FcgammaRIIA leads to membrane rafts coalescing into signaling platforms containing PIP5-kinase Ialpha and PI(4,5)P(2).
PIP5K1alpha was found to be required for AKT activation and calcium release, both of which were important for skeletal muscle differentiation.
these results support that PIP5Kalpha can positively mediate TLR2-associated immune responses through Phosphatidylinositol 4,5-bisphosphate production in microglial cells.
Data suggest that c-Fos (proto-oncogene protein c-fos; not c-Jun) regulates phospholipid synthesis in cell nucleus; c-Fos localizes to nucleus and modulates genetic transcription through activation of Pip5k1.
optimal PIP5KIgamma and PI(4,5)P(2) expression, by osteoclasts, are essential for skeletal homeostasis
Our findings suggest that PI4P5Kalpha plays a complex role in restricting insulin release from pancreatic beta-cells through helping to maintain plasma membrane PIP(2) levels and integrity of the actin cytoskeleton under both basal and stimulatory conditions.
The results suggested that PIP5K1A and PIP5K1B may coordinately and/or redundantly function in the maintenance of sperm number and morphology during spermatogenesis.
mPIP5K-Ibeta acts through PI(4,5)P2 to regulate endosomal trafficking and/or fusion.
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
that membrane turnover events regulating ENaC surface expression and activity in oocytes and CCD cells can be regulated by PI5KIalpha.
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
PIP5K-Ialpha may play an important role in both the proximal and distal steps of signaling cascade for insulin secretion in beta-cells.
Data indicate a structural motif unique to the kinase family that serves to recognize the monophosphate on the substrate in type I kinase PIP5Kalpha.
Pip5k1a activity is regulated by dimerization and binding with the DIX domain of dishevelled.
Catalyzes the phosphorylation of phosphatidylinositol 4- phosphate (PtdIns4P) to form phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2). PtdIns(4,5)P2 is involved in a variety of cellular processes and is the substrate to form phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P3), another second messenger. The majority of PtdIns(4,5)P2 is thought to occur via type I phosphatidylinositol 4-phosphate 5-kinases given the abundance of PtdIns4P. Participates in a variety of cellular processes such as actin cytoskeleton organization, cell adhesion, migration and phagocytosis. Required for membrane ruffling formation, actin organization and focal adhesion formation during directional cell migration by controlling integrin-induced translocation of RAC1 to the plasma membrane. Together with PIP5K1C is required for phagocytosis, but they regulate different types of actin remodeling at sequential steps. Promotes particle ingestion by activating WAS that induces Arp2/3 dependent actin polymerization at the nascent phagocytic cup. Together with PIP5K1B is required after stimulation of G-protein coupled receptors for stable platelet adhesion. Plays a role during calcium-induced keratinocyte differentiation. Recruited to the plasma membrane by the E-cadherin/beta-catenin complex where it provides the substrate PtdIns(4,5)P2 for the production of PtdIns(3,4,5)P3, diacylglycerol and inositol 1,4,5-trisphosphate that mobilize internal calcium and drive keratinocyte differentiation. Together with PIP5K1C have a role during embryogenesis. Functions also in the nucleus where acts as an activator of TUT1 adenylyltransferase activity in nuclear speckles, thereby regulating mRNA polyadenylation of a select set of mRNAs.
68 kDa type I phosphatidylinositol 4-phosphate 5-kinase alpha
, 68 kDa type I phosphatidylinositol-4-phosphate 5-kinase alpha
, phosphatidylinositol 4-phosphate 5-kinase type I alpha
, phosphatidylinositol 4-phosphate 5-kinase type-1 alpha
, phosphatidylinositol-4-phosphate 5-kinase type-1 alpha
, ptdIns(4)P-5-kinase 1 alpha
, phosphatidylinositol-4-phosphate 5-kinase, type 1 beta
, phosphatidylinositol-4-phosphate 5-kinase, type I, alpha
, phosphatidylinositol-4-phosphate 5-kinase, type I, beta
, 68 kDa type I phosphatidylinositol 4-phosphate 5-kinase
, 68 kDa type I phosphatidylinositol-4-phosphate 5-kinase
, phosphatidylinositol 4-phosphate 5-kinase type I beta
, phosphatidylinositol-4-phosphate 5-kinase type I alpha
, phosphatidylinositol-4-phosphate 5-kinase type I beta
, phosphatidylinositol-4-phosphate 5-kinase type-1 gamma