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JAK2 — PI3

Text-mined interactions from Literome

Al-Shami et al., J Biol Chem 1999 : These results suggest that stimulation of the activity of PI3-kinase induced by GM-CSF is mediated by Jak2 and that the association between Jak2 and p85 depends on an adaptor protein yet to be identified
Miike et al., J Leukoc Biol 1999 : These results indicate that activation of JAK2 , but not activation of PI 3-kinase/Akt and MAP kinase pathways, is critical for anti-apoptotic signals of GM-CSF in human eosinophils
Song et al., Chin J Cancer 2002 (Multiple Myeloma) : IL-6 inhibited apoptosis of XG-7 cells through up-regulation of Mcl-1 and the activation of JAK/STAT rather than Ras/MAPK nor PI-3K/Akt signal transduction pathway
Carino et al., Int J Cancer 2008 (Adenocarcinoma...) : Leptin induction of cytokines/receptors generally involved JAK2 and MAPK activation, but PI-3K phosphorylation was required for leptin increase of LIF, IL-1/IL-1R tI
Girasol et al., PloS one 2009 : Surprisingly, some of these effects are dependent on signal transduction through the IRS1/PI3-kinase , but not on the activation of JAK2
Aksamitiene et al., Cell Signal 2011 (Breast Neoplasms) : The specific blockade or siRNA mediated suppression of SFK/FAK, JAK2/STAT5, PI3-kinase/PDK1/Akt, Rac/PAK or Ras regulatory circuits revealed that ( 1 ) the PI3-kinase/Akt pathway is required for activation of the MAPK/ERK signaling cascade upon PRL stimulation ; ( 2 ) PI3-kinase mediated activation of the c-Raf-MEK1/2-ERK1/2 cascade occurs independent of signaling dowstream of STATs, Akt and PKC, but requires JAK2 , SFKs and FAK activities ; ( 3 ) activated PRL-R mainly utilizes the PI3-kinase dependent Rac/PAK pathway rather than the canonical Shc/Grb2/SOS/Ras route to initiate and sustain ERK1/2 signaling
Britschgi et al., Cancer Cell 2012 (Breast Neoplasms...) : Mechanistically, PI3K/mTOR inhibition increased IRS1 dependent activation of JAK2/STAT5 and secretion of IL-8 in several cell lines and primary breast tumors
Xu et al., Int J Mol Med 2013 : In another set of cultures, the cells were co-incubated with RTB and the tyrosine kinase inhibitor, genistein, the phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, the p42/44 inhibitor, PD98059, the p38 inhibitor, SB203580, the JNK inhibitor, SP600125, the protein kinase C ( PKC ) inhibitor, staurosporine, the JAK2 inhibitor , tyrphostin ( AG490 ), or the NOS inhibitor, L-NMMA
Oh et al., J Biol Chem 1998 : Moreover, JAK1 binds to PI 3-kinase, and LIF stimulation increases the PI 3-kinase activity in JAK1 immunoprecipitates