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INPP5D is a member of the inositol polyphosphate-5-phosphatase (INPP5) family and encodes a protein with an N-terminal SH2 domain, an inositol phosphatase domain, and two C-terminal protein interaction domains. Additionally we are shipping Inositol Polyphosphate-5-Phosphatase, 145kDa Kits (9) and Inositol Polyphosphate-5-Phosphatase, 145kDa Proteins (3) and many more products for this protein.
Showing 10 out of 106 products:
Human Monoclonal INPP5D Primary Antibody for FACS - ABIN2662843
Banh, Miah, Kerr, Brossay: Mouse natural killer cell development and maturation are differentially regulated by SHIP-1. in Blood 2012
Show all 5 references for ABIN2662843
Human Monoclonal INPP5D Primary Antibody for FACS, WB - ABIN302081
Ai, Maturu, Johnson, Wang, Marsh, Tridandapani: The inositol phosphatase SHIP-2 down-regulates FcgammaR-mediated phagocytosis in murine macrophages independently of SHIP-1. in Blood 2006
Show all 4 references for ABIN302081
Human Monoclonal INPP5D Primary Antibody for EIA, WB - ABIN238500
Xing, Hamaguchi: Effects of SHIP-1 on MMP2 secretion and invasion of SR3Y1 cells. in Journal of genetics and genomics = Yi chuan xue bao 2007
Show all 4 references for ABIN238500
Mouse (Murine) Monoclonal INPP5D Primary Antibody for IF, WB - ABIN968479
Lioubin, Algate, Tsai, Carlberg, Aebersold, Rohrschneider: p150Ship, a signal transduction molecule with inositol polyphosphate-5-phosphatase activity. in Genes & development 1996
Show all 3 references for ABIN968479
Human Polyclonal INPP5D Primary Antibody for EIA, WB - ABIN358021
Gilby, Goodeve, Winship, Valk, Delwel, Reilly: Gene structure, expression profiling and mutation analysis of the tumour suppressor SHIP1 in Caucasian acute myeloid leukaemia. in Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 2007
Show all 3 references for ABIN358021
Human Polyclonal INPP5D Primary Antibody for ELISA, WB - ABIN1531473
Ware, Rosten, Damen, Liu, Humphries, Krystal: Cloning and characterization of human SHIP, the 145-kD inositol 5-phosphatase that associates with SHC after cytokine stimulation. in Blood 1996
Our results describe a critical role for SHIP-1 in regulating the ability of dendritic cells to efficiently prime Th2-type responses.
Findings indicate a role for inositol-polyphosphate 5-phosphatase SHIP-1 coupling to DC-type lectin receptor ectin-1 hemITAM in the selective control of downstream responses.
miR (show MLXIP Antibodies)-155 regulates the delicate balance between PAK1 (show PAK1 Antibodies)-mediated proliferation and apoptosis in T cells impacting lymphoid organ size and function.
miR (show MLXIP Antibodies)-155 regulation of SHIP represents a unique axis that regulates dendritic cells function in vivo.
SHIP1 and Csk (show CSK Antibodies) are part of the PSTPIP2 (show PSTPIP2 Antibodies)-dependent inhibitory network that prevents the development of autoinflammatory disease.
intracellular signaling by SHIP1 in mesenchymal stem cells is critical for hematopoiesis and lineage commitment during aging.
Data show that 5'-inositol phosphatase SHIP1 deficiency extrinsically affects invariant NK (iNKT) cell proliferation.
Selective deletion of Ship1 in T cells or dendritic cells impairs the formation of an adaptive TH2 response and protects animals from house dust mite-induced allergic airway inflammation.
SHIP1 regulates mesenchymal stem cell numbers and their osteolineage commitment by limiting induction of the PI3K/Akt (show AKT1 Antibodies)/beta-catenin (show CTNNB1 Antibodies) pathways
by promoting survival of protective T cells, thereby preventing an inflammatory myeloid response, SHIP1 maintains an appropriate balance of innate immune function at mucosal surfaces necessary for immune homeostasis.
SHIP levels and activity are lower in intestinal tissues and peripheral blood samples from patients with Crohn's disease, resulting in induction of Il1-beta (show IL1B Antibodies).
Underexpression of SHIP1 is associated with drug resistance in acute myeloid leukemia (show BCL11A Antibodies).
ectopically expressed SHIP1 accumulates in nucleolar cavities and colocalizes with the tumor suppressor protein p53 (show TP53 Antibodies).
Results show that expression of SHIP1 protein is targeted by miR (show MLXIP Antibodies)-155 in acute myeloid leukemia (show BCL11A Antibodies) (AML (show RUNX1 Antibodies)) suggesting it as an onco-miR (show MLXIP Antibodies). The miR (show MLXIP Antibodies)-155/SHIP1/PI3K (show PIK3CA Antibodies)/AKT (show AKT1 Antibodies) signaling pathway could play an important role in the pathogenesis of AML (show RUNX1 Antibodies).
Overexpression of miR (show MLXIP Antibodies)-155 in the gouty synovial fluid mononuclear cells leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.
SLAMF7 (show SLAMF7 Antibodies)-triggered inhibition is mediated by a mechanism involving Src (show SRC Antibodies) kinases, CD45 (show PTPRC Antibodies), and SHIP-1 that is defective in MM cells
The discovery and replication studies presented here show SHIP-1 to be a risk marker for acute ischemic stroke in the Chinese population, which appears to be a novel finding.
High ship1 expression is associated with chronic lymphocytic leukemia.
Tks5 (show SH3PXD2A Antibodies) is needed for breast carcinoma cell invadopodium precursor stabilization, where the phox homology (PX) domain of Tks5 (show SH3PXD2A Antibodies) interacts with PI(3,4)P2. SHIP2 (show INPPL1 Antibodies) arrival at the invadopodium precursor coincides with the onset of PI(3,4)P2 accumulation.
Based on these observations, authors conclude that miR (show MLXIP Antibodies)-155 modulates the neuroinflammatory response during Japanese encephalitis virus infection via negative regulation of SHIP1 expression.
This gene is a member of the inositol polyphosphate-5-phosphatase (INPP5) family and encodes a protein with an N-terminal SH2 domain, an inositol phosphatase domain, and two C-terminal protein interaction domains. Expression of this protein is restricted to hematopoietic cells where its movement from the cytosol to the plasma membrane is mediated by tyrosine phosphorylation. At the plasma membrane, the protein hydrolyzes the 5' phosphate from phosphatidylinositol (3,4,5)-trisphosphate and inositol-1,3,4,5-tetrakisphosphate, thereby affecting multiple signaling pathways. Overall, the protein functions as a negative regulator of myeliod cell proliferation and survival. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
inositol polyphosphate-5-phosphatase, 145kDa
, SH2 containing inositol phosphatase
, phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase 1
, phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase 1-like
, SH2 domain-containing inositol 5'-phosphatase 1
, SH2 domain-containing inositol phosphatase 1
, SH2 domain-containing inositol-5'-phosphatase 1
, phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 1
, Phosphatidylinositol-3,4,5-trisphosphate 5-phosphatase 1
, SH2 containing inositol phosphotase
, SH2-containing inositol phosphatase SHIP
, Src homology 2 domain-containing inositol-5-phosphatase
, inositol polyphosphate-5-phosphatase of 145 kDa
, inositol polyphosphate-5-phosphatase, 145 kDa
, Inositol polyphosphate-5-phosphatase 145 kDa
, Inositol polyphosphate-5-phosphatase, 145 kDa
, signaling inositol polyphosphate 5 phosphatase SIP-145