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BCL2 — IL3

Text-mined interactions from Literome

Dumon et al., Oncogene 1999 : IL-3 dependent regulation of Bcl-xL gene expression by STAT5 in a bone marrow derived cell line
Deng et al., Proc Natl Acad Sci U S A 2000 : High concentrations of stauro of up to 1 microM only partially inhibit IL-3 stimulated Bcl2 phosphorylation but completely block PKC mediated Bcl2 phosphorylation in vitro ... A role for a MEK/MAPK as a responsible SRK was implicated because the highly specific MEK/MAPK inhibitor, PD98059, also can only partially inhibit IL-3 induced Bcl2 phosphorylation, whereas the combination of PD98059 and stauro completely blocks phosphorylation and synergistically enhances apoptosis
Re et al., J Hematother Stem Cell Res 2000 : In addition, using an interleukin-3 dependent TF-1 cell line, it was demonstrated that IL-3 deprivation was sufficient to influence the levels of telomerase activity and Bcl-2 expression in CD34+ cells
Deng et al., J Natl Cancer Inst Monogr 2001 (Leukemia, Myeloid...) : However, we have recently found that high concentrations of staurosporine up to 1 microM : can only partially inhibit IL-3 stimulated Bcl2 phosphorylation but completely block PKCalpha mediated Bcl2 phosphorylation in vitro, indicating the existence of a non-PKC, staurosporine-resistant Bcl2 kinase ( SRK )
Deng et al., J Biol Chem 2001 : Interleukin (IL)-3 induced Bcl2 phosphorylation at Ser ( 70 ) may be required for its full and potent antiapoptotic activity
Karlsson et al., J Leukoc Biol 2003 : Phosphatidylinositol 3-kinase is essential for kit ligand mediated survival, whereas interleukin-3 and flt3 ligand induce expression of antiapoptotic Bcl-2 family genes ... We next established if IL-3 and FL activated antiapoptotic Bcl-2 and the related genes Bcl-XL and Mcl-1 ... By RNA protection assay and Western blot analysis, we show that all three genes are induced by IL-3 , whereas FL induces Bcl-2 and to some extent Bcl-XL
Nuñez et al., J Immunol 1990 : Overexpressed Bcl-2 resulted in no long term IL-2, IL-3 , or IL-6 independent clones, indicating that Bcl-2 could not spare the need for a specific ligand-receptor interaction
Cleveland et al., Oncogene 1994 : Surprisingly, steady state levels of Bcl-2 , an oncogene known to suppress apoptosis, were not dependent upon IL-3 in 32D.3 cells and its levels were not augmented in v-raf clones