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These results show that SHIP-1 is required for the maintenance of B10 cells and production of IL-10 (show IL10 ELISA Kits), and collectively suggests that SHIP-1 could be a new potential therapeutic target for the treatment of autoimmune diseases.
Rictor (show RICTOR ELISA Kits) positively regulates B cell receptor signaling via up-regulating Btk (show BTK ELISA Kits) and down-regulating SH2-containing inositol phosphatase
MiR (show MLXIP ELISA Kits)-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 (show AKT1 ELISA Kits)/CTGF (show CTGF ELISA Kits) signaling in diabetic kidney dise
this study shows that FcgammaRIIb drives the sequential dephosphorylation system comprising SHIP1/2 and Inpp4a (show INPP4A ELISA Kits), and accelerates phagosome acidification
Data (including data from studies in knockout mice) suggest that up-regulation of signaling in colonic mucosa via interleukin-10 (show IL10 ELISA Kits)/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 (show MLXIP ELISA Kits)-155 regulates the delicate balance between PAK1 (show PAK1 ELISA Kits)-mediated proliferation and apoptosis in T cells impacting lymphoid organ size and function.
JARID1B directly bound to PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits) 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 (show ATG16L1 ELISA Kits), 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 (show SYK ELISA Kits)-dependent mechanisms may be an important factor modulating immunoreceptor signaling.
SHIP has a role in extracellular matrix accumulation via suppressing PI3K (show PIK3CA ELISA Kits)/Akt (show AKT1 ELISA Kits)/CTGF (show CTGF ELISA Kits) 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 (show IL1B ELISA Kits).
Underexpression of SHIP1 is associated with drug resistance in acute myeloid leukemia (show BCL11A ELISA Kits).
ectopically expressed SHIP1 accumulates in nucleolar cavities and colocalizes with the tumor suppressor protein p53 (show TP53 ELISA Kits).
Results show that expression of SHIP1 protein is targeted by miR (show MLXIP ELISA Kits)-155 in acute myeloid leukemia (show BCL11A ELISA Kits) (AML (show RUNX1 ELISA Kits)) suggesting it as an onco-miR (show MLXIP ELISA Kits). The miR (show MLXIP ELISA Kits)-155/SHIP1/PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits) signaling pathway could play an important role in the pathogenesis of AML (show RUNX1 ELISA Kits).
Overexpression of miR (show MLXIP ELISA Kits)-155 in the gouty synovial fluid mononuclear cells leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.
SLAMF7 (show SLAMF7 ELISA Kits)-triggered inhibition is mediated by a mechanism involving Src (show SRC ELISA Kits) kinases, CD45 (show PTPRC ELISA Kits), 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