Identifiers
HUGO:PTPN11
protein tyrosine phosphatase, non-receptor type 11
HUGO:PTPN11 hgnc_id:HGNC:9644 HGNC:9644 ENTREZ:5781 UNIPROT:Q06124
"Noonan syndrome 1", NS1
HUGO:PTPN11 HGNC:9644 ENTREZ:5781 UNIPROT:Q06124
Maps_Modules
HMC:AVOIDING_IMMUNE_DESTRUCTION
Adaptive Immune Response / INHIBITING_CHECKPOINTS
HMC:TUMOR_PROMOTING_INFLAMMATION
HMC:ACTIVATING_INVASION_AND_METASTASIS
Cancer Associated Fibroblasts / CORE
EMT Senescence / CELL_CELL_ADHESIONS
EMT Senescence / ADHERENS_JUNCTIONS
Innate Immunity / IMMUNOSTIMULATORY_CYTOKINE_PATHWAYS
Innate Immunity / IMMUNOSUPPPRESSIVE_CORE_PATHWAYS
References
PMID:11572860 PMID:15240681
CASCADE:FGF
PMID:11447289
Tyrosine-phosphorylated Shp2 molecules have not been detected in FRS2?? mutant cell lysates, indicating that FRS2?? is required for tyrosine phosphorylation of Shp2 leading to complex formation between Shp2 and Grb2. FGF-induced tyrosine phosphorylation of Shp2 as well as FRS2??/Grb2 complex formation were completely restored by ectopic expression of FRS2?? in mutant cells. These findings demonstrate that expression of functional FRS2?? is indeed crucial for the recruitment and tyrosine phosphorylation of these two effector proteins
CASCADE:KIR2DL3
CASCADE:KIR2DL2
CASCADE:KIR2DL1
CASCADE:NKG2A
CASCADE:KIR3DL1
CASCADE:KIR2DL4
CASCADE:2B4
NATURAL_KILLER
MACROPHAGE
PMID:19833085, PMID:15699106, PMID:12138178
Inactivation of nuclear STAT1 occurs rapidly following binding to chromatin and activation of target gene transcription.
Subsequently STAT1 is dephosphorylated by phosphatases such as PTPN2 (TCP45) and PTPN11 (SHP2), and dephosphorylated STAT1
PMID:10358138, PMID:15713798
Human 2B4 is phosphorylated following activation and recruits PTPN11 (SHP-2). Association of SAP with h2B4 prevents recruitment of SHP-2.
PMID:12707331
There is direct correlation between SHP-2 recruitment and functional inhibition of target cell conjugation and cytotoxicity downstream of KIR3DL.
PMID:9751747
KIR2DL3, KIR2DL1, KIR2DS4, KIR3DL1, KIR3DL2, KIR2DL4 interact with SHP-2 in NK cells
and probably are phosphorylated by LCK (directly demonstrated for KIR2DL3 only).
(CL6 = KIR2DL3,CL42 =KIR2DL1, CL39 = KIR2DS4, NKAT3= KIR3DL1, NKAT4 = KIR3DL2,KIR103AS=KIR2DL4) .
References
in_re709( Innate Immunity ):
PMID:19833085, PMID:15699106, PMID:12138178, PMID:12270932
Inactivation of nuclear STAT1 occurs rapidly following binding to chromatin and activation of target gene transcription.
Subsequently STAT1 is dephosphorylated by phosphatases such as PTPN2 (TCP45) and PTPN11 (SHP2), and dephosphorylated STAT1
returns to cytoplasm, where it can potentially serve as the substrate for subsequent rounds of activation and inactivation.
PMID:19833085
Probably, acetylation of STAT1 on lysine residues 410 and 413 in the nucleus results in enhanced interaction with TCP45 (PTPN2) and increased dephosphorylation
in_re712( Innate Immunity ):
PMID:19833085, PMID:15699106, PMID:15699106, PMID:15699106