SHIP1*

Protein SHIP1*

Maps_Modules
HMC:AVOIDING_IMMUNE_DESTRUCTION
Adaptive Immune Response / INHIBITING_CHECKPOINTS
HMC:TUMOR_PROMOTING_INFLAMMATION
Innate Immunity / IMMUNOSUPPPRESSIVE_CORE_PATHWAYS
Innate Immunity / IMMUNOSTIMULATORY_CORE_PATHWAYS

References
PMID:22483603 PMID:12421919
MACROPHAGE
MAST_CELL
NATURAL_KILLER
CASCADE:IL4
CASCADE:IL10
CASCADE:FCGR2B
CASCADE:2B4
CASCADE:SLAMF7
CASCADE:Fc_gamma_RII
CASCADE:Fc_gamma_RIII
PMID:22483603
SH2-domain containing inositol-5-phosphatase (SHIP) de-phosphorylates PI(3,4,5)P3 at the D5 position of the inositol ring to create PI(3,4)P2.
PMID:15713798
The phosphorylated third ITSM of 2B4 can recruit the phosphatases SHP-1, SHP-2, SHIP, and the inhibitory kinase Csk. SAP acts as an inhibitor of interactions between 2B4 and these negative regulatory molecules, explaining how 2B4 inhibits NK-cell activation in the absence of functional SAP.
PMID:15169881
2B4 signaling induces phosphorylation of SHIP1,VAV1,CBL.
This phosphorylation is dependent on SAP and FYN.
PMID:22683124
2B4-mediated inhibition was restored when SHIP-1 was reintroduced in SHIP-1-deficient cells.
In the NK cells lacking SHIP-1, there was a prominent diminution of the inhibitory influence of 2B4 (to ???25% of control).
PMID:12393695
CD16 stimulation on human primary natural killer (NK) cells induces the rapid and transient translocation of SHIP-1 in the lipid-enriched plasma membrane microdomains, termed rafts, where it associates with tyrosine-phosphorylated zeta chain and shc adaptor protein.
SHIP1 inhinits NK cells activation via bloking of PI3K pathway. It hydrolyzes the 5???-phosphate of PI3,4,5P3l eading to its conversion to PI3,4P2.
PMID:20363967, PMID:16204085
Src homology 2-containing inositol 5'-phosphatase 1 negatively regulates IFN-gamma production by natural killer cells stimulated with antibody-coated tumor cells and interleukin-12, probably via inhibition of PI3K pathway and downstream ERK signaling.
PMID:11449354, PMID:12393695
CD16 cross-linking on human NK cells induces the association of SHIP-1 with receptor zeta-chain through the adaptor protein shc.
Fc gamma RIII alpha (CD16) autoregulates activation of downstream signals trough CD3 zeta/ Shc/ Inositol polyphosphate-5-phosphatase 145kDa ( SHIP ) pathway. The hypothetical mechanism consists of SHIP participation in inhibition of Ca('2+) -depend pathway and signal from PI3K via decreased amount IP3 [45] and PtdIns(3,4,5)P3.
PMID:1238444
FcgammaRIIa-mediated phagocytosis was significantly enhanced in THP-1 cells overexpressing dominant-negative form of SHIP in the absence of FcgammaRII(b). These results indicate that SHIP negatively regulates FcgammaR-mediated phagocytosis through all ITAM-containing IgG receptors
PMID:20435894
IL-10 inhibits miR-155 expression via STAT3. 3--UTR of SHIP1 is targeted by miR-155. Inhibition of Mir155 expression upregulates SHIP downstream of IL10
PMID:22955274
SHIP inhibit MAPKp38 activation and prevent MNK1 phosphorylation by inhibiting the p38 MAPK pathway downstream of IL10. MNK1 regulates TNFa mRNA polysome assembly and upregulates TNFa translation.IL-10 Inhibits TNF Translation through SHIP1-mediated Inhibition of Mnk1
PMID:21469115
IL4 signaling reduces SHIP protein levels and activity via PI3K correlating with M2 marker induction ( activation of arginase protein level and activity and inhibition of NO production).

SHIP1*|pho|active@INNATE_IMMUNE_CELL_Cytosol

References
in_re930( Innate Immunity ):
PMID:11875494
IL10-induced p38 phosphorylation.
PMID:20435894
SHIP inhibit MAPKp38 activation and prevent
MKNK1 phosphorylation by inhibiting the p38MAPK
pathway downstream of IL10.
PMID:10925299
IL13 induces p38 MAPK phosphorilation and activation, p38 MAPK participates in arginase activation??downstream of IL13.
PMID:23508573
HMGB1 induces activation (phosphorylation) of p38 via TLR4.
PMID:12811837, PMID:16713974
TLR signaling can induces STAT1 phosphorylation via p38 and potentiate IFNG signaling.
PMID:16713974
TLR2 activates (induces phosphorylation of) ERKs, JNKs, and p38 rapidly and transiently in control macrophages.
This activation is inhibited by IFNG signaling.
PMID:11438547, PMID:24378531
Both TNFR1 and TNFR2 signaling pathways are needed for activation of p38 MAPK.

Modifications:
In compartment: INNATE_IMMUNE_CELL_Cytosol

SHIP1*@INNATE_IMMUNE_CELL_Cytosol
SHIP1*|pho|active@INNATE_IMMUNE_CELL_Cytosol

Participates in complexes:
In compartment: INNATE_IMMUNE_CELL_Cytosol

SHC1|pho:SHIP1*|pho@INNATE_IMMUNE_CELL_Cytosol

Participates in reactions:
As Reactant or Product:

As Catalyser: