Phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 2 (INPPL1)
Links to databases
Phosphatidylinositol (PtdIns) phosphatase that specifically hydrolyzes the 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) to produce PtdIns(3,4)P2, thereby negatively regulating the PI3K (phosphoinositide 3-kinase) pathways. Plays a central role in regulation of PI3K-dependent insulin signaling, although the precise molecular mechanisms and signaling pathways remain unclear. While overexpression reduces both insulin-stimulated MAP kinase and Akt activation, its absence does not affect insulin signaling or GLUT4 trafficking. Confers resistance to dietary obesity. May act by regulating AKT2, but not AKT1, phosphorylation at the plasma membrane. Part of a signaling pathway that regulates actin cytoskeleton remodeling. Required for the maintenance and dynamic remodeling of actin structures as well as in endocytosis, having a major impact on ligand-induced EGFR internalization and degradation. Participates in regulation of cortical and submembraneous actin by hydrolyzing PtdIns(3,4,5)P3 thereby regulating membrane ruffling (PubMed:21624956). Regulates cell adhesion and cell spreading. Required for HGF-mediated lamellipodium formation, cell scattering and spreading. Acts as a negative regulator of EPHA2 receptor endocytosis by inhibiting via PI3K-dependent Rac1 activation. Acts as a regulator of neuritogenesis by regulating PtdIns(3,4,5)P3 level and is required to form an initial protrusive pattern, and later, maintain proper neurite outgrowth. Acts as a negative regulator of the FC-gamma-RIIA receptor (FCGR2A). Mediates signaling from the FC-gamma-RIIB receptor (FCGR2B), playing a central role in terminating signal transduction from activating immune/hematopoietic cell receptor systems. Involved in EGF signaling pathway. Upon stimulation by EGF, it is recruited by EGFR and dephosphorylates PtdIns(3,4,5)P3. Plays a negative role in regulating the PI3K-PKB pathway, possibly by inhibiting PKB activity. Down-regulates Fc-gamma-R-mediated phagocytosis in macrophages independently of INPP5D/SHIP1. In macrophages, down-regulates NF-kappa-B-dependent gene transcription by regulating macrophage colony-stimulating factor (M-CSF)-induced signaling. May also hydrolyze PtdIns(1,3,4,5)P4, and could thus affect the levels of the higher inositol polyphosphates like InsP6. Involved in endochondral ossification.
Recommended sample types are human EDTA plasma and serum. A range of additional sample types are compatible with the technology (PEA), including citrate plasma, heparin plasma, cerebrospinal fluid, (CSF), tissue and cell lysates, fine needle biopsis, microdialysis fluid, cell culture media, dried blood spots, synovial fluid, saliva, plaque extract and microvesicles. Please note that protein expression levels are expected to vary in different sample types. Certain assays are differentially affected by interfering substances such as hemolysate. Download any of our Data Validation documents or contact firstname.lastname@example.org for more information.
NOTE: The calibrator curve below shows the performance of the assay with the estimated sensitivity and dynamic range parameters indicated. These curves are generated during the assay validation process using recombinant antigens. Please note that when analyzing biological samples the data generated will be given in the form of relative quantification (NPX values) and cannot be converted to absolute protein concentrations. For more info about NPX measurements, please visit our FAQ page.
Analytical Measuring Range
Calibrator curve for validation data (generated in multiplex)
- Within run precision Coefficient of Variation (CV)
- Between run precision Coefficient of Variation (CV)
Precision (repeatability) is calculated from linearized NPX values over LOD.
Biomarker Validation Data
Additional validation data, as well as a more detailed description of how the Olink panels are quality controlled can be found in our Data Validation documents. To download or to learn more go to the Data Validation page.