|Other Names||Phosphatidylinositol 3, 5-trisphosphate 5-phosphatase 1, Inositol polyphosphate-5-phosphatase of 145 kDa, SIP-145, SH2 domain-containing inositol 5'-phosphatase 1, SH2 domain-containing inositol phosphatase 1, SHIP-1, p150Ship, hp51CN, INPP5D, SHIP, SHIP1|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP8473b was selected from the C-term region of human hSHIP1. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||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. Acts as a negative regulator of B-cell antigen receptor signaling. Mediates signaling from the FC-gamma-RIIB receptor (FCGR2B), playing a central role in terminating signal transduction from activating immune/hematopoietic cell receptor systems. Acts as a negative regulator of myeloid cell proliferation/survival and chemotaxis, mast cell degranulation, immune cells homeostasis, integrin alpha-IIb/beta-3 signaling in platelets and JNK signaling in B-cells. Regulates proliferation of osteoclast precursors, macrophage programming, phagocytosis and activation and is required for endotoxin tolerance. Involved in the control of cell-cell junctions, CD32a signaling in neutrophils and modulation of EGF-induced phospholipase C activity. Key regulator of neutrophil migration, by governing the formation of the leading edge and polarization required for chemotaxis. Modulates FCGR3/CD16-mediated cytotoxicity in NK cells. Mediates the activin/TGF-beta-induced apoptosis through its Smad-dependent expression. May also hydrolyze PtdIns(1,3,4,5)P4, and could thus affect the levels of the higher inositol polyphosphates like InsP6.|
|Cellular Location||Cytoplasm. Membrane; Peripheral membrane protein. Note=Translocates to the plasma membrane 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) or CD16/FCGR3. Tyrosine phosphorylation may also participate in membrane localization (By similarity)|
|Tissue Location||Specifically expressed in immune and hematopoietic cells. Expressed in bone marrow and blood cells Levels vary considerably within this compartment. Present in at least 74% of immature CD34+ cells, whereas within the more mature population of CD33+ cells, it is present in only 10% of cells Present in the majority of T-cells, while it is present in a minority of B-cells (at protein level)|
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Provided below are standard protocols that you may find useful for product applications.
SHIP1, SH2-containing inositol phosphatase 1, hydrolyzes phosphatidylinositol-3,4,5-triphosphate to phosphatidylinositol-3,4-bisphosphate. SHIP1 is a cytosolic phosphatase that affects calcium flux, cell survival, growth, cell cycle arrest, and apoptosis mediated through the PI3K and Akt pathways. SHIP1 is a negative regulator B lymphoid cell, myeloid cell, and mast cell activation.
Maxwell, M., et al. 2004. J. Biol. Chem. 279, 32196. Giuriato, S., et al. 2003. Biochem. J. 376, 199. Sly, L.M., at al. 2003. Exp. Hematol. 31, 1170. Sattler, M., et al. 2001. J. Biol. Chem. 276, 2451.
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