Product Pathways - Ca / cAMP / Lipid Signaling
INPP4b (D19B9) Rabbit mAb #8450
|8450S||100 µl (10 western blots)||---||In Stock||---|
|8450||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse||Endogenous||110||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation
Specificity / Sensitivity
INPP4b (D19B9) Rabbit mAb recognizes endogenous levels of total INPP4b protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human INPP4b protein.
Phosphotidylinositol lipids and phosphoinositides are important second messengers, their generation controlling many cellular events. Intracellular levels of these molecules are regulated by phosphoinositide kinases and phosphatases. One of the best characterized lipid kinases is phosphoinositide 3-kinase (PI3K), which is responsible for phosphorylation on the D-3 position of the inositide head group (1). This action of PI3K catalyzes the production of phosphatidylinositol-3,4,5-triphosphate by phosphorylating phosphatidylinositol (PI), phosphatidylinositol-4-phosphate (PIP), and phosphatidylinositol-4,5-bisphosphate (PIP2). Growth factors and hormones trigger this phosphorylation event, which in turn coordinates cell growth, cell cycle entry, cell migration, and cell survival (1). PTEN, the well characterized partnering phosphatase, reverses this process by removing the phosphate from PI(3,4,5)P3 at the D-3 position to generate PI(4,5)P2 (1,2). Dephosphorylation on the D-5 position to generate PI(3,4)P2 occurs through the action of SHIP1 or SHIP2 (3), and dephosphorylation on the D-4 position to generate PI(3)P can occur through the action of inositol polyphosphate 4-phosphatase isoenzymes type I (INPP4a) and type II (INPP4b) (4,5). While INPP4a has been implicated in neuronal survival and megakaryocyte lineage determination (6,7), less is understood about INPP4b. It has been shown that two splice variants of INPP4b occur in mice, each showing distinct tissue distribution and subcellular localization (5,8).
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