PIP5K1A Antibody

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.

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.

Store at 4˚ C for three months and -20˚ C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

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