Product nameAnti-INPPL1/SHIP-2 antibody [EPR10954]
See all INPPL1/SHIP-2 primary antibodies
DescriptionRabbit monoclonal [EPR10954] to INPPL1/SHIP-2
Tested applicationsSuitable for: WB, Flow Cyt, IPmore details
Unsuitable for: ICC or IHC-P
Species reactivityReacts with: Mouse, Rat, Human
Synthetic peptide corresponding to Human INPPL1/SHIP-2.
Database link: O15357
- Daudi, HeLa and K562 cell lysates; Permeabilized K562 cells.
Previously labelled as INPPL1.
This product is a recombinant monoclonal antibody, which offers several advantages including:
- - High batch-to-batch consistency and reproducibility
- - Improved sensitivity and specificity
- - Long-term security of supply
- - Animal-free production
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
Storage instructionsShipped at 4°C. Store at -20ºC.
Storage bufferPreservative: 0.01% Sodium azide
Constituents: 9% PBS, 40% Glycerol, 0.05% BSA, 50% Tissue culture supernatant
Concentration information loading...
PurityTissue culture supernatant
Our Abpromise guarantee covers the use of ab157460 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000 - 1/10000. Predicted molecular weight: 139 kDa.|
|Flow Cyt||1/10 - 1/100.
ab172730 - Rabbit monoclonal IgG, is suitable for use as an isotype control with this antibody.
|IP||1/10 - 1/100.|
FunctionPhosphatidylinositol (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. 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.
Tissue specificityWidely expressed, most prominently in skeletal muscle, heart and brain. Present in platelets. Expressed in transformed myeloid cells and in primary macrophages, but not in peripheral blood monocytes.
Involvement in diseaseDefects in INPPL1 may be a cause of susceptibility to type 2 diabetes mellitus non-insulin dependent (NIDDM) [MIM:125853].
Note=Genetic variations in INPPL1 may be a cause of susceptibility to metabolic syndrome. Metabolic syndrome is characterized by diabetes, insulin resistance, hypertension, and hypertriglyceridemia is absent.
Sequence similaritiesBelongs to the inositol 1,4,5-trisphosphate 5-phosphatase family.
Contains 1 SAM (sterile alpha motif) domain.
Contains 1 SH2 domain.
DomainThe SH2 domain interacts with tyrosine phosphorylated forms of proteins such as SHC1 or FCGR2A. It also mediates the interaction with p130Cas/BCAR1.
The NPXY sequence motif found in many tyrosine-phosphorylated proteins is required for the specific binding of the PID domain.
modificationsTyrosine phosphorylated by the members of the SRC family after exposure to a diverse array of extracellular stimuli such as insulin, growth factors such as EGF or PDGF, chemokines, integrin ligands and hypertonic and oxidative stress. May be phosphorylated upon IgG receptor FCGR2B-binding. Phosphorylated at Tyr-986 following cell attachment and spreading. Phosphorylated at Tyr-1162 following EGF signaling pathway stimulation. Phosphorylated at Thr-958 in response to PDGF.
Cellular localizationCytoplasm > cytosol. Cytoplasm > cytoskeleton > actin patch. Membrane. Translocates to membrane ruffles when activated, translocation is probably due to different mechanisms depending on the stimulus and cell type. Partly translocated via its SH2 domain which mediates interaction with tyrosine phosphorylated receptors such as the FC-gamma-RIIB receptor (FCGR2B). Tyrosine phosphorylation may also participate in membrane localization. Insulin specifically stimulates its redistribution from the cytosol to the plasma membrane. Recruited to the membrane following M-CSF stimulation.
- Information by UniProt
- 4 antibody
- 5-trisphosphate 5-phosphatase 2 antibody
- 51C protein antibody
Lane 1: Wild-type HAP1 whole cell lysate (20 µg)
Lane 2: INPPL1/SHIP-2 knockout HAP1 whole cell lysate (20 µg)
Lane 3: HeLa whole cell lysate (20 µg)
Lane 4: K562 whole cell lysate (20 µg)
Lanes 1 - 4: Merged signal (red and green). Green - ab157460 observed at 139 kDa. Red - loading control, ab9484, observed at 37 kDa.
ab157460 was shown to specifically react with INPPL1/SHIP-2 in wild-type HAP1 cells. No bands were observed when INPPL1/SHIP-2 knockout samples were examined. Wild-type and INPPL1/SHIP-2 knockout samples were subjected to SDS-PAGE. Ab157460 and ab9484 (Mouse anti GAPDH loading control) were incubated overnight at 4°C at 1/1000 dilution and 1/10000 dilution respectively. Blots were developed with Goat anti-Rabbit IgG H&L (IRDye® 800CW) preabsorbed ab216773 and Goat anti-Mouse IgG H&L (IRDye® 680RD) preabsorbed ab216776 secondary antibodies at 1/10000 dilution for 1 hour at room temperature before imaging.
Flow cytometric analysis of permeabilized K562 cells labeling INPPL1/SHIP-2 with ab157460 at 1/10 dilution (red) or a rabbit IgG (negative) (green).
All lanes : Anti-INPPL1/SHIP-2 antibody [EPR10954] (ab157460) at 1/1000 dilution
Lane 1 : Daudi cell lysate
Lane 2 : Hela cell lysate
Lane 3 : K562 cell lysate
Lysates/proteins at 10 µg per lane.
All lanes : Goat anti-rabbit HRP at 1/2000 dilution
Predicted band size: 139 kDa
Detection of INPPL1/SHIP-2 by Western Blot of Immunprecipitate. HeLa cell lysate immunoprecipitated using ab157460 at 1/10 dilution.
Anti-INPPL1/SHIP-2 antibody [EPR10954] (ab157460) at 1/1000 dilution + immunoprecipitation pellet from HeLa cell lysate
ab157460 has not yet been referenced specifically in any publications.