Gene interactions and pathways from curated databases and text-mining

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IL2 — PIK3R1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Ciprés et al., Eur J Immunol 1999 : The requirement for IL-2 induced PI3K activity in suppressing the onset of apoptotic cell death is discussed
Harada et al., J Biol Chem 2001 : In contrast, the N191A mutant, which retains PI3K binding ability, resulted in a complete abrogation of activity, suggesting that PI3K mediates a negative effect upon transcriptional activation of the IL-2 gene ... Taken together, these data indicate that PI3K , when associated with the YMNM motif, may act as a negative mediator in CD28 mediated IL-2 gene transcription
Phu et al., J Leukoc Biol 2001 : IL-2 synthesis by anti-CD3 activated CD8 ( + ) T cells was also diminished by PI3-K inhibition ... These results support the conclusion that PI3-K activation is involved in T-cell receptor, CD28, and IL-2 receptor signaling of CD8 ( + ) T cells
Heijink et al., Eur J Immunol 2003 : Together, our results indicate that increased IL-2 dependent PI3-K signaling leads to impaired negative feedback control of the production of Th2-type cytokine IL-5 by the cAMP dependent pathway
Chakraborty et al., Neuroscience 2003 : Activation of PI3K by IL-2 was also blocked by tyrphostin A25, a selective inhibitor of PTK, suggesting activation of the latter by IL-2 is upstream to PI3K activation
Williams et al., J Immunol 2004 (Disease Susceptibility...) : Inhibition of PI3K resulted in increased serum levels of IL1-beta, IL-2 , IL-6, IL-10, IL-12, and TNF-alpha in septic mice
Brando-Lima et al., Int Immunopharmacol 2006 : This effect is inhibited by D-galactose and PI3K inhibitors, and is accompanied by an increase in IL-2 receptor expression and by a PI3K dependent IL-2 gene expression and IL-2 protein synthesis
Sanchez-Lockhart et al., J Immunol 2006 : CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription
Marzec et al., Blood 2008 (Lymphoma, T-Cell, Cutaneous) : The mTORC1, PI3K/Akt , and MEK/ERK pathways could also be activated by IL-2 in the primary leukemic, mitogen preactivated CTCL cells
Venkatachalam et al., Am J Physiol Heart Circ Physiol 2008 (Hyperglycemia) : Resveratrol inhibits high glucose induced PI3K/Akt/ERK dependent interleukin-17 expression in primary mouse cardiac fibroblasts
Zheng et al., J Immunol 2008 (HIV Infections) : We demonstrate that IL-2 initially requires both STAT5 and PI3K activation to increase expression of IL-2Rbeta, produce granulysin, and kill C. neoformans
Gentle et al., J Immunol 2012 : Modulation required de novo protein synthesis, and PI3K , JNK, and ERK activity were necessary for enhanced IL-2 expression, whereas modulation of IL-10 required only PI3K activity
Monfar et al., Mol Cell Biol 1995 : We demonstrate that these kinases lie on the same signalling pathway and that PI3K mediates the activation of pp70 by the cytokine interleukin-2 (IL-2) ... Like rapamycin, PKA appears to act downstream of cPKC mediated pp70S6k activation, and like wortmannin, PKA antagonizes IL-2 dependent activation of PI3K
Ghiotto-Ragueneau et al., Eur J Immunol 1996 : Worthmannin, a specific inhibitor of PI3-K enzymatic activity within the nanomolar range also inhibits the interleukin-2 production induced by costimulation mediated by either the B7.1- and B7.2 transfected cells or CD28 monoclonal antibodies
Bavelloni et al., J Cell Sci 1999 (Osteosarcoma) : Phosphatidylinositol 3-kinase translocation to the nucleus is induced by interleukin 1 and prevented by mutation of interleukin 1 receptor in human osteosarcoma Saos-2 cells