Gene interactions and pathways from curated databases and text-mining

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PIK3R1 — PTPN11

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Wu et al., Oncogene 2000 (Brain Neoplasms...) : Reduced EGF stimulated activation of PI3-K was mediated by interactions between carboxyl terminus of SIRPalpha1 and the Src homology-2 (SH2) containing phosphotyrosine phosphatase, SHP2 ... These data reveal a pathway that negatively regulates EGFR induced PI3-K activation in glioblastoma cells and involves interactions between SHP2 and tyrosine phosphorylated SIRPalpha1
Yart et al., J Biol Chem 2001 : Indeed, the association of Gab1 with SHP2 was blocked by PI3K inhibitors, and expression of Gab1 mutant deficient for binding to SHP2 was found to inhibit Ras stimulation without interfering with PI3K activation
Wu et al., Oncogene 2001 (Glioblastoma) : Based on these results, we conclude that SHP-2 is required for mediating PI3K/Akt activation, and the N-terminal SH2 domain is critically important for a `` positive '' role of SHP-2 in regulating PI3K pathway activation
Zhang et al., Mol Cell Biol 2002 : Our results suggest that, in addition to its role as a positive component of the Ras-Erk pathway, Shp2 negatively regulates EGF dependent PI3K activation by dephosphorylating Gab1 p85 binding sites, thereby terminating a previously proposed Gab1-PI3K positive feedback loop
Hale et al., Proc Natl Acad Sci U S A 2006 : Additionally, it was found that expression of NS1 alone was sufficient to constitutively activate PI3K , causing the phosphorylation of a downstream mediator of PI3K signal transduction, Akt
Ehrhardt et al., J Virol 2007 : NS1 binds to and activates PI3K , which results in the activation of the PI3K effector Akt
Sampaio et al., Mol Cell Biol 2008 : Indeed, by up- and down-regulation of signal strength in different cell lines and through different methods, we observed that Gab1/Shp2 and Ras/ERK1-2 in concert become independent of PI3K upon strong epidermal growth factor receptor (EGFR) stimulation and dependent on PI3K upon limited EGFR activation
Hale et al., J Biol Chem 2008 : Overall, these data suggest a model by which NS1 activates PI3K catalytic activity by masking a normal regulatory element specific to the p85beta inter-SH2 domain
Gallacher et al., J Physiol 2009 (Influenza, Human) : This response to virus infection was only partially dependent upon NS1 mediated activation of PI3K
Jackson et al., Virology 2010 : Surprisingly, given previous reports that NS1 activates PI3K to prevent apoptosis, the mutant viruses rUd-Y89F and rUd-P164/7A that fail to activate PI3K did not induce any more apoptosis than wild-type virus in MRC-5 and A549 cells, even though these cells are highly sensitive to inducers of apoptosis
Hale et al., Proc Natl Acad Sci U S A 2010 : Overall, these data suggest that both direct binding of NS1 to p85beta ( resulting in repositioning of the N-terminal SH2 domain ) and possible NS1 : p110 contacts contribute to PI3K activation