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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