Identifiers
HUGO:PIK3R1 HUGO:PIK3R2
phosphoinositide-3-kinase regulatory subunit 1
HUGO:PIK3R1 hgnc_id:HGNC:8979 HGNC:8979 ENTREZ:5295 UNIPROT:P27986
phosphoinositide-3-kinase regulatory subunit 2
HUGO:PIK3R2 hgnc_id:HGNC:8980 HGNC:8980 ENTREZ:5296 UNIPROT:O00459
Maps_Modules
HMC:AVOIDING_IMMUNE_DESTRUCTION
Adaptive Immune Response / TCR_SIGNALING
HMC:TUMOR_PROMOTING_INFLAMMATION
HMC:ACTIVATING_INVASION_AND_METASTASIS
Cancer Associated Fibroblasts / CORE
Innate Immunity / IMMUNOSTIMULATORY_CORE_PATHWAYS
References
PMID:12670391 PMID:11526404 PMID:23087689
CASCADE:PDGF
CASCADE:FGF
CASCADE:GAST
PMID:23523669
Progastrin-induced secretion of insulin-like growth factor 2 from colonic myofibroblasts stimulates colonic epithelial proliferation in mice.
Incubation of CCD18Co myofibroblasts with 0.1 nmol/L rhPG(1-80) increased their proliferation, which required activation of protein kinase C and phosphatidylinositol-3 kinase.
PMID:24751819
PMID:11687500
The class IA PI3Ks, which transmit signals from tyrosine kinase-coupled receptors, are heterodimeric proteins having a p110 catalytic subunit associated with a p85, p55, or p50 regulatory subunit.
PMID:7682895; PMID:17397400
PDGF -receptor directly binds and activates PLC-gamma 1, RasGAP, P13K, and a 64 kd protein.
PI3K-Akt pathway promotes microtubule stabilization in migrating fibroblasts downstream of PDGF signaling
PMID:11447289
FGF-induced stimulation of PI-3 kinase activity in Gab1 immunoprecipitates from wild-type fibroblasts. By contrast, PI-3 kinase activity was not detected in Gab1 immunoprecipitates from FGF-stimulated FRS2??-deficient fibroblasts. However, stimulation of PI-3 kinase was completely restored by ectopic expression of FRS2?? cDNA in FRS2??-deficient fibroblasts (Fig. ???(Fig.33C). These experiments demonstrate that FRS2?? functions as a site of assembly of an additional docking protein that brings to the complex its own effectors in addition to the effectors that bind directly to FRS2??.
NATURAL_KILLER
MACROPHAGE
NEUTROPHIL
DENDRITIC_CELL
MAST_CELL
CASCADE:LGALS3
CASCADE:IL4
CASCADE:SLAMF7
CASCADE:NKP80
CASCADE:NKG2D
CASCADE:NKP46
CASCADE:Fc_gamma_RIII
CASCADE:IL15
CASCADE:IL21
CASCADE:CSF2
CASCADE:IFNAB
CASCADE:IFNG
IL21 signaling activates PI3K/AKT pathway
PMID:11062502, PMID:11385609, PMID:11907067, PMID:15536084
Nkp46 controls NK cytolitic activity via PI3K /RAC1/PAK1/MEK??/ERK pathway, probably throught SYK
PMID:18250477
Galectin-3 mediate alternative activation of macrophages via activation of PI3K signaling and AKT posphorylation. And regulates expression of MRC1 probably via PI3K
PMID:11907067, PMID:15536084
SYK kinaze directly interacts with PI3K(p85) and activates perforin ??granule movement and polarization via PI3K /RAC1/PAK1/MEK??/ERK pathway
PMID:10426994, 16582911??
Phosphorylated DAP10 directly interacts with regulatory subunit (p85) of PI3K and activates downstream pathway.
PMID:18287025
NKG2D-mediated cytotoxicity is PI3K-dependent.
PMID:21149606
NKp80-mediated cytotoxicity is PI3K-dependent.
PMID:24795729
IL15 induces IFNG production via PI3K/AKT/MTOR pathway.
PI3K???AKT???mTOR pathway is required for granzyme B production downstream of IL15.
Treatment with PI3K inhibitor abrogated the priming effect. Such inhibition was also observed
with blocking mTOR and AKT, downstream signaling components of PI3K pathway,
suggesting that PI3K???AKT???mTOR pathway is critical for optimal responses of ???primed??? NK cells to cytokine stimulations.
PMID:9314552
Syk- macrophages exhibited formation of polymerized actin structures opposing particles bound to the cells by FcgammaRs (actin cups), but failed to proceed to internalization. Interestingly, inhibitors of phosphatidylinositol 3-kinase also blocked FcgammaR-mediated phagocytosis at this stage. Thus, PI 3-kinase may participate in a Syk-dependent signaling pathway critical for FcgammaR-mediated phagocytosis.
PMID:19109239
IL4 induces he tyrosine phosphorylation of IRS-2 via Type I IL-4 Receptors. Activated IRS2 interacts with p85 subunit of PI3K and Grb2 and activates downstrean PI3K signaling (??phosphorylation of Akt on Ser473)
PMID:20805416
In differentiating moDCs, the PI3K/Akt-dependent mTOR pathway was constitutively activated by GM-CSF
And this signaling is needful for DC differentiation.
PMID:25960930
IFN?? induces PKC-?? auto-phosphorylation in NK cells via P3K and PLC pathways and improves the degranulation via PKC-?? signaling
PMID:16713974, PMID:11579131
INFG pathway inhibits activation (phosphorylation) of ERK, JNK, p38 kinases and PI3K pathway induced by TLR. Inhibition of AKT pathway by IFNG resulted in activation of GSK3. GSK3 inhibits downstream AP-1 and CREB1 signaling and downregulates IL10 expression induced by TLR.IFNG inhibits CREB activation via p38 induced by TLR signaling
PMID:19909365
MAST cells
PMID:21826665
TLR4/PI3K signaling in TAN promotes motility of cancer cells
References
in_re163( Innate Immunity ):
PMID:16713974
TLR signaling activates and IFNG inhibits PI3K pathway
PMID:11907067, PMID:15536084
SYK kinaze directly interacts with PI3K(p85) and activates perforin ??granule movement and polarization via PI3K /RAC1/PAK1/MEK??/ERK pathway
PMID:10426994??
Phosphorylated DAP10 directly interacts with regulatory subunit (p85) of PI3K and activates downstream pathway.
→ PI3KR(p85)*@INNATE_IMMUNE_CELL_Cytosol
+ PI3KR(p85)*@INNATE_IMMUNE_CELL_Cytosol → CRKL:PI3KR(p85)*@INNATE_IMMUNE_CELL_Cytosol
→ rMRC1@MARKERS_MACROPHAGE
→ p110*@INNATE_IMMUNE_CELL_Cytosol
+ RAPGEF1@INNATE_IMMUNE_CELL_Cytosol + CBL|pho|active@INNATE_IMMUNE_CELL_Cytosol + CRK@INNATE_IMMUNE_CELL_Cytosol + CRKL@INNATE_IMMUNE_CELL_Cytosol → (BCAR1|pho:CBL|pho:CRK:CRKL:RAPGEF1)|active@INNATE_IMMUNE_CELL_Cytosol