Browse our anti-Inositol Polyphosphate-5-Phosphatase, 145kDa (INPP5D) Antibodies

Zebrafish Inositol Polyphosphate-5-Phosphatase, 145kDa (INPP5D) interaction partners

1. SHIP phosphatases control neutrophil inflammation by limiting neutrophil motility in vivo.

Mouse (Murine) Inositol Polyphosphate-5-Phosphatase, 145kDa (INPP5D) interaction partners

1. We investigated the role of SHIP1 as a tumor suppressor in myeloid leukemia cells in an in vivo xenograft transplantation model. The AML-derived SHIP1Y643H mutant, which has a strongly reduced enzymatic activity showed significant reversion of SHIP1-induced prolongation of the survival time. In addition, analysis of 290 patients revealed a correlation between expression of SHIP1 and overall survival of the AML patients.

2. High SHIP1 expression is associated with lymphoma and colon cancer.

3. These results show that SHIP-1 is required for the maintenance of B10 cells and production of IL-10, and collectively suggests that SHIP-1 could be a new potential therapeutic target for the treatment of autoimmune diseases.

4. Rictor positively regulates B cell receptor signaling via up-regulating Btk and down-regulating SH2-containing inositol phosphatase

5. MiR-155 promotes experimental colitis by repressing SHIP-1 expression.

6. Results are consistent with predicted/observed reduction in the Lyn-SHIP-1-PTEN-SHP-1 axis function in B cells from systemic lupus

7. SHIP has a role in extracellular matrix accumulation via suppressing PI3K/Akt/CTGF signaling in diabetic kidney dise

8. this study shows that FcgammaRIIb drives the sequential dephosphorylation system comprising SHIP1/2 and Inpp4a, and accelerates phagosome acidification

9. Data (including data from studies in knockout mice) suggest that up-regulation of signaling in colonic mucosa via interleukin-10/microRNA-155/SHIP-1 (Src homology 2 domain-containing inositol-5-phosphatase) is involved in development of colitis due to dysbiosis.

10. Our results describe a critical role for SHIP-1 in regulating the ability of dendritic cells to efficiently prime Th2-type responses.

11. 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.

12. miR-155 regulates the delicate balance between PAK1-mediated proliferation and apoptosis in T cells impacting lymphoid organ size and function.

13. miR-155 regulation of SHIP represents a unique axis that regulates dendritic cells function in vivo.

14. SHIP1 and Csk are part of the PSTPIP2-dependent inhibitory network that prevents the development of autoinflammatory disease.

15. intracellular signaling by SHIP1 in mesenchymal stem cells is critical for hematopoiesis and lineage commitment during aging.

16. Data show that 5'-inositol phosphatase SHIP1 deficiency extrinsically affects invariant NK (iNKT) cell proliferation.

17. 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.

18. SHIP1 regulates mesenchymal stem cell numbers and their osteolineage commitment by limiting induction of the PI3K/Akt/beta-catenin pathways

19. 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.

20. Overexpression of miR-155 in the gouty synovial fluid mononuclear cells leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.

Human Inositol Polyphosphate-5-Phosphatase, 145kDa (INPP5D) interaction partners

1. On title.

2. Overall evidence did not indicate that inositol polyphosphate-5-phosphatase (INPP5D) rs35349669 single nucleotide polymorphism play a role in the genetic predisposition to late-onset Alzheimer's disease (LOAD) in Chinese population.

3. JARID1B directly bound to PI3K/AKT signaling inhibitor SHIP1 gene promoter and decreased SHIP1 gene expression.

4. 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, SHIP1 may contribute to the risk conferred by the 2q37 CD risk locus.

5. 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-dependent mechanisms may be an important factor modulating immunoreceptor signaling.

6. SHIP has a role in extracellular matrix accumulation via suppressing PI3K/Akt/CTGF signaling in diabetic kidney dise

7. Loss of SHIP promotes lung inflammation and mammary tumor metastasis.

8. 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.

9. Underexpression of SHIP1 is associated with drug resistance in acute myeloid leukemia.

10. ectopically expressed SHIP1 accumulates in nucleolar cavities and colocalizes with the tumor suppressor protein p53.

11. Results show that expression of SHIP1 protein is targeted by miR-155 in acute myeloid leukemia (AML) suggesting it as an onco-miR. The miR-155/SHIP1/PI3K/AKT signaling pathway could play an important role in the pathogenesis of AML.

12. Overexpression of miR-155 in the gouty synovial fluid mononuclear cells leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.

13. SLAMF7-triggered inhibition is mediated by a mechanism involving Src kinases, CD45, and SHIP-1 that is defective in MM cells

14. 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.

15. High ship1 expression is associated with chronic lymphocytic leukemia.

16. Tks5 is needed for breast carcinoma cell invadopodium precursor stabilization, where the phox homology (PX) domain of Tks5 interacts with PI(3,4)P2. SHIP2 arrival at the invadopodium precursor coincides with the onset of PI(3,4)P2 accumulation.

17. Based on these observations, authors conclude that miR-155 modulates the neuroinflammatory response during Japanese encephalitis virus infection via negative regulation of SHIP1 expression.

18. SHIP1 silencing opposes TIGIT/PVR-mediated inhibitory signaling and restores cytotoxicity of YTS cells.

19. Mutation in the PxxP domain of SHIP affects cell migration and invasion ability of K562 cells through increased MMP-9 expression, FAK phosphorylation and NF-kappaB activation.

20. inositol phosphatase SHIP-1 inhibits NOD2-induced NF-kappaB activation by disturbing the interaction of XIAP with RIP2