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These results show that SHIP-1 is required for the maintenance of B10 cells and production of IL-10 (显示 IL10 ELISA试剂盒), and collectively suggests that SHIP-1 could be a new potential therapeutic target for the treatment of autoimmune diseases.
Rictor (显示 RICTOR ELISA试剂盒) positively regulates B cell receptor signaling via up-regulating Btk (显示 BTK ELISA试剂盒) and down-regulating SH2-containing inositol phosphatase
MiR (显示 MLXIP ELISA试剂盒)-155 promotes experimental colitis by repressing SHIP-1 expression.
Results are consistent with predicted/observed reduction in the Lyn-SHIP-1-PTEN-SHP-1 axis function in B cells from systemic lupus
SHIP has a role in extracellular matrix accumulation via suppressing PI3K/Akt (显示 AKT1 ELISA试剂盒)/CTGF (显示 CTGF ELISA试剂盒) signaling in diabetic kidney dise
this study shows that FcgammaRIIb drives the sequential dephosphorylation system comprising SHIP1/2 and Inpp4a (显示 INPP4A ELISA试剂盒), and accelerates phagosome acidification
Data (including data from studies in knockout mice) suggest that up-regulation of signaling in colonic mucosa via interleukin-10 (显示 IL10 ELISA试剂盒)/microRNA-155/SHIP-1 (Src homology 2 domain-containing inositol-5-phosphatase) is involved in development of colitis due to dysbiosis.
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 (显示 MLXIP ELISA试剂盒)-155 regulates the delicate balance between PAK1 (显示 PAK1 ELISA试剂盒)-mediated proliferation and apoptosis in T cells impacting lymphoid organ size and function.
JARID1B directly bound to PI3K (显示 PIK3CA ELISA试剂盒)/AKT (显示 AKT1 ELISA试剂盒) signaling inhibitor SHIP1 gene promoter and decreased SHIP1 gene expression.
Study shows that SHIP1 activity is decreased in adult Crohn's disease (CD) patients either through reduced intrinsic enxymatic activity or reduced protein expression, and propose that in addition to ATG16L1 (显示 ATG16L1 ELISA试剂盒), SHIP1 may contribute to the risk conferred by the 2q37 CD risk locus.
results indicate that FcgammaRIIB is not uniquely able to promote membrane recruitment of SHIP, but rather modulates its function via formation of distinct signaling complexes. Membrane recruitment of SHIP via Syk (显示 SYK ELISA试剂盒)-dependent mechanisms may be an important factor modulating immunoreceptor signaling.
SHIP has a role in extracellular matrix accumulation via suppressing PI3K (显示 PIK3CA ELISA试剂盒)/Akt (显示 AKT1 ELISA试剂盒)/CTGF (显示 CTGF ELISA试剂盒) signaling in diabetic kidney dise
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 (显示 IL1B ELISA试剂盒).
Underexpression of SHIP1 is associated with drug resistance in acute myeloid leukemia (显示 BCL11A ELISA试剂盒).
ectopically expressed SHIP1 accumulates in nucleolar cavities and colocalizes with the tumor suppressor protein p53 (显示 TP53 ELISA试剂盒).
Results show that expression of SHIP1 protein is targeted by miR (显示 MLXIP ELISA试剂盒)-155 in acute myeloid leukemia (显示 BCL11A ELISA试剂盒) (AML (显示 RUNX1 ELISA试剂盒)) suggesting it as an onco-miR (显示 MLXIP ELISA试剂盒). The miR (显示 MLXIP ELISA试剂盒)-155/SHIP1/PI3K (显示 PIK3CA ELISA试剂盒)/AKT (显示 AKT1 ELISA试剂盒) signaling pathway could play an important role in the pathogenesis of AML (显示 RUNX1 ELISA试剂盒).
Overexpression of miR (显示 MLXIP ELISA试剂盒)-155 in the gouty synovial fluid mononuclear cells leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.
SLAMF7 (显示 SLAMF7 ELISA试剂盒)-triggered inhibition is mediated by a mechanism involving Src (显示 SRC ELISA试剂盒) kinases, CD45 (显示 PTPRC ELISA试剂盒), and SHIP-1 that is defective in MM cells
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