Gene interactions and pathways from curated databases and text-mining

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CSF1 — PI3

Text-mined interactions from Literome

Murray et al., J Cell Sci 2000 : The inhibition of vesicle trafficking and maturation correlated with ablation of M-CSF induced PI-3 kinase activity associated with p110(alpha)
Gobert Gosse et al., Cell Signal 2005 (MAP Kinase Signaling System) : Therefore, M-CSF differentiation signaling in myeloid progenitor cells is mediated through persistent MEK activity but it is not strictly dependent upon Grb2-Sos interaction or PI 3-kinase activity
Wang et al., Am J Respir Cell Mol Biol 2007 : M-CSF induces PI 3-kinase activation, resulting in reactive oxygen species ( ROS ) production
Reedijk et al., Mol Cell Biol 1990 (Chromosome Deletion) : These results indicate that the kinase insert region selectively enhances the CSF-1 dependent association of the CSF-1 receptor with active PI 3'-kinase
Saleem et al., J Biol Chem 1995 : In the present studies, we demonstrate that M-CSF also induces direct interaction of PI 3-kinase ( p85 alpha subunit ) with the SH2/SH3 adaptor protein Grb2
Yusoff et al., Growth Factors 1994 : The results demonstrate that CSF-1 increases the activity of PI 3-kinase , as compared to the non stimulated control, in murine macrophages
Reith et al., Oncogene 1993 (Cell Transformation, Neoplastic) : Moreover, expression of Fms37 or Fms42 proteins in Rat-2 cells specifically inhibited anchorage independent growth mediated by the normal Fms receptor in the presence of exogenous CSF-1 and conferred a dominant loss of Fms associated PI3-kinase activity on CSF-1 stimulation
Bourette et al., EMBO J 1997 : Since the Fms Y807F mutation abrogates the differentiation signal when expressed in FDC-P1 cells and since this phenotype could be reproduced by a specific inhibitor of PLC-gamma, we propose that a balance between the activities of PLC-gamma2 and PI3-kinase in response to M-CSF is required for cell differentiation
Kanagasundaram et al., Biochem J 1998 : Even though CSF-1 induced PI 3-kinase activity in both BMM and RPM, wortmannin, a potent inhibitor of PI 3-kinase activity, at concentrations that inhibited PI 3-kinase activity by 90 % in these cells, had little or no effect on receptor internalization and degradation in either BMM or RPM or on CSF-1 degradation by BMM