- CITATIONS: 2
|Application ||WB, E|
|Calculated MW||62633 Da|
|Antigen Region||19-50 aa|
|Other Names||Phosphatidylinositol 4-phosphate 5-kinase type-1 alpha, PIP5K1-alpha, PtdIns(4)P-5-kinase 1 alpha, 68 kDa type I phosphatidylinositol 4-phosphate 5-kinase alpha, Phosphatidylinositol 4-phosphate 5-kinase type I alpha, PIP5KIalpha, PIP5K1A|
|Target/Specificity||This PIP5K1A antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 19-50 amino acids from the N-terminal region of human PIP5K1A.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||PIP5K1A Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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.|
|Cellular Location||Cell membrane. Cytoplasm. Nucleus speckle. Cell projection, ruffle. Note=Colocalizes with RAC1 at actin-rich membrane ruffles. Localizes to nuclear speckles and associates with TUT1 to regulate polyadenylation of selected mRNAs|
|Tissue Location||Highly expressed in heart, placenta, skeletal muscle, kidney and pancreas. Detected at lower levels in brain, lung and liver|
Provided below are standard protocols that you may find useful for product applications.
Overexpression of phosphatidylinositol phosphate 5-kinase alpha (PIP5KIalpha), which synthesizes PIP2, suppresses apoptosis, whereas a kinase-deficient mutant does not. Protection by the wild-type PIP5KIalpha isaccompanied by decreases in the generation of activated caspases and of caspase 3-cleaved PARP. Protection is not mediated through PIP3 or Akt activation. An anti-apoptotic role for PIP(2) is substantiated by the finding that PIP5KIalpha is cleaved by caspase 3 during apoptosis, and cleavage inactivates PIP5KIalpha in vitro. Mutation of the P(4) position (D279A) of the PIP5KIalpha caspase 3 cleavage consensus prevents cleavage in vitro, and during apoptosis in vivo. Significantly, the caspase 3-resistant PIP5KIalpha mutant is more effective in suppressing apoptosis than the wild-type kinase. PIP2 is a direct regulator of apical and effector caspases in the death receptor and mitochondrial pathways, and PIP5KIalpha inactivation contributes to the progression of apoptosis.
Doughman, R.L., et al., J. Biol. Chem. 278(25):23036-23045 (2003).
Loijens, J.C., et al., J. Biol. Chem. 271(51):32937-32943 (1996).
Xie, Y., et al., Cytogenet. Cell Genet. 88 (3-4), 197-199 (2000).
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