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AKT1 — IL3

Text-mined interactions from Literome

Craddock et al., J Biol Chem 1999 : Expression of Deltap85 reduces IL-3 induced PKB phosphorylation and activation and phosphorylation of BAD dramatically, to levels seen in unstimulated cells
Le et al., J Biol Chem 2000 (MAP Kinase Signaling System) : Moreover, the mutations abolished IL-3 induced JAK2, STAT, and AKT activation in the unselected cells, whereas activation of these molecules in IL-3 selected cells was normal
Gu et al., Mol Cell Biol 2000 (Precursor B-Cell Lymphoblastic Leukemia-Lymphoma) : The majority of cytokine stimulated PI-3K activity associates with Gab2, and inducible expression of a Gab2 mutant unable to bind PI-3K markedly impairs IL-3 induced Akt activation and cell growth
Zirngibl et al., Mol Cell Biol 2002 : Bone marrow derived Fps/Fes-null macrophages showed no defects in granulocyte-macrophage colony stimulating factor-, interleukin 6 (IL-6)-, or IL-3 induced activation of signal transducer and activator of transcription 3 ( Stat3 ) and Stat5A or LPS induced degradation of I kappa B or activation of p38, Jnk, Erk, or Akt
Burgess et al., J Neuroimmunol 2003 : However, only IL-3 and IGF-I increase enzymatic activity and phosphorylation of the survival promoting kinase Akt
Wheadon et al., Blood 2003 : Induction of TEL/PDGFbetaR expression led to increased cell survival following IL-3 withdrawal and constitutive activation of protein kinase B (PKB) , signal transducer and activator of transcription 5 ( STAT5 ), extracellular signal regulated kinases 1/2 ( ERK1/2 ), Jun N-terminal kinases 1/2 (JNK1/2), and p38 mitogen activated protein kinase ( MAPK ) pathways ... We demonstrate that TEL/PDGFbetaR expression augmented IL-3 induced activation of PKB , STAT5, ERK1/2, p38, and JNK1/2
Wheadon et al., Biochem J 2003 : Expression of WT, C459S and D425A forms of SHP-2 had little effect on IL-3-driven proliferation or STAT5 ( signal transduction and activators of transcription ) phosphorylation or activation of protein kinase B
Luo et al., Zhonghua Xue Ye Xue Za Zhi 2004 (Leukemia, Myeloid, Acute...) : In addition, in vitro Akt phosphorylation was prolonged and increased following IL-3 stimulation of this patient 's cells
Luo et al., Zhongguo Shi Yan Xue Ye Xue Za Zhi 2004 (Leukemia, Myeloid, Acute...) : In addition, Akt phosphorylation was prolonged and increased following IL-3 stimulation in this patient sample
Okamura et al., Life Sci 2006 : Contrary to KN-CKIepsilon, WT-CKIepsilon attenuated the IL-3 induced activation of Akt with the increase of PTEN activity
Edmead et al., Cell Signal 2006 : Expression of DeltaPHGab-2 reduced IL-3 dependent proliferation and long-term activation of ERK1 and 2 and PKB by IL-3
Qi et al., J Biol Chem 2006 (Carcinoma, Hepatocellular) : The PI3K inhibitor, LY294002, blocked IL-3 stimulated Akt activity and partially blocked Bim ( EL ) phosphorylation
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
Hidano et al., Int Immunol 2012 : Biochemical analyses revealed that IL-3 induced phosphorylation of phospholipase C (PLC) ?2 and Akt , but not STAT5, was severely reduced in SLP-76-deficient basophils, whereas FceRI cross linking phosphorylation of PLC?2, but not Akt, was abrogated by SLP-76 deficiency, suggesting important differences in the requirement of SLP-76 for Akt activation between FceRI- and IL-3 receptor mediated signaling pathways in basophils
Songyang et al., Proc Natl Acad Sci U S A 1997 : We find that Akt kinase activity is rapidly induced by the cytokine IL-3 , suggesting a role for Akt in PI 3-kinase dependent signaling in hematopoetic cells
del Peso et al., Science 1997 : Akt , a survival promoting serine-threonine protein kinase, was activated by IL-3 in a PI 3-kinase dependent manner