Gene interactions and pathways from curated databases and text-mining

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PIK3R1 — SRC

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

Amyere et al., Int J Med Microbiol 2002 : v-Src and K-Ras activate PI3K and PLC, as demonstrated by in situ production of the corresponding lipid products
Bock et al., J Biol Chem 2003 : Here we demonstrate that PI3K activation by Reelin requires Src family kinase activity and depends on the Reelin triggered interaction of Dab1 with the PI3K regulatory subunit p85alpha
Shenoy et al., J Immunol 2003 : We conclude that MBP stimulates a Src kinase dependent activation of class I ( A ) PI3K and, in turn, activation of PKCzeta in neutrophils, which contributes to the activation of NADPH oxidase and the resultant O ( 2 ) ( - ) production in response to MBP stimulation
Carini et al., Gastroenterology 2004 (Reperfusion Injury) : PI3K is activated following hepatocyte hypoxic preconditioning by the combined stimulation of adenosine A 2A receptors, PKA, Galphai protein, and Src
Facchini et al., FEBS Lett 2005 : In turn Src can activate PI3K and PKC-delta, and all these signaling proteins are required for ODC induction
Díaz-Montero et al., Eur J Cancer 2006 (Osteosarcoma) : PI3-K/Akt mediated anoikis resistance of human osteosarcoma cells requires Src activation
Arcaro et al., Cell Signal 2007 (Carcinoma, Small Cell) : Together our data demonstrate that lipid rafts play a key role in the activation of PI3K signalling by facilitating the interaction of Src with specific PI3K isoforms
Thamilselvan et al., FASEB J 2007 (Colonic Neoplasms...) : PI3K inhibitor ( LY294002 ) prevented pressure stimulated Akt Ser473 and FAK Tyr397, but not FAK576 or Src416 phosphorylation
Jin et al., Cancer Res 2007 (Cell Transformation, Neoplastic) : Suppression of c-Src by RNA interference in NIH3T3-ETV6-NTRK3 cells resulted in markedly decreased expression of cyclin D1 and suppression of activation of Ras-Erk1/2 and PI3K-Akt
Jin et al., J Biol Chem 2008 (Cell Transformation, Neoplastic) : Suppression of c-Src by RNA interference in highly metastatic 4T1 mammary cancer cells, which express endogenous TrkC, resulted in markedly decreased expression of cyclin D1 and suppression of activation of Ras-Erk1/2 and PI3K-Akt
Lin et al., Toxicol Appl Pharmacol 2008 : LPS stimulated Src , PYK2, EGFR, and Akt phosphorylation and VCAM-1 expression were attenuated by the inhibitors of Src ( PP1 ), EGFR ( AG1478 ), PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110
Gingerich et al., Neuropharmacology 2008 : Finally, we demonstrate that Src kinase acts upstream of the PI3K/Akt pathway based on our finding that the selective Src inhibitor, PP2 ( 10microM ), blocked the increases in nNOS phosphorylation levels, NO production, and PI3K/Akt activity induced by ERbeta activation
Meng et al., Br J Cancer 2009 (Adenocarcinoma...) : In addition, the Src inhibitor, PP2, blocked the phosphorylation of FAK, ERK1/2, PI3K , and Akt
Jiang et al., J Biol Chem 2010 (Prostatic Neoplasms) : Basal tyrosine phosphorylation of p110beta and p110delta could be blocked by c-Src inhibitors, but this did not suppress PI3K activity, which was similarly independent of Ras
Lei et al., Am J Physiol Lung Cell Mol Physiol 2011 : In summary, in adult rat AECs T3-stimulated Src kinase activity can activate both PI3K/Akt and MAPK/ERK1/2, and activation of Akt is necessary for T3-induced Na-K-ATPase activity
Lin et al., Science signaling 2011 : These phosphorylation events enabled direct binding of GIV to the amino- and carboxyl-terminal Src homology 2 domains of p85a, a regulatory subunit of PI3K ; stabilized receptor association with PI3K ; and enhanced PI3K activity at the plasma membrane to trigger cell migration
Samoylenko et al., Carcinogenesis 2012 (Adenocarcinoma...) : Thereby, Ruk ( l ) /CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of Src , Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility
Busch et al., J Biol Chem 2012 : IL-1ß induced NF-?B and PI3K activation was inhibited by resveratrol or the inhibitors of PI3K ( wortmannin ), c-Src ( PP1 ), and Akt ( SH-5 ) through inhibition of I?B kinase, I?Ba phosphorylation, and inhibition of nuclear translocation of NF-?B, suggesting that PI3K signaling pathway may be one of the signaling pathways inhibited by resveratrol to abrogate NF-?B activation