Colony stimulating factor-1 ( @entity9827 or @entity9827 ) is the major physiological regulator of the proliferation, differentiation and survival of cells of the mononuclear phagocyte lineage. @entity9827 binds to a receptor @entity669 kinase, the @entity17224 ( @entity17224 ). Multiple pathways are activated downstream of the @entity17224 ; however, it is not clear which pathways regulate proliferation and survival. Here, we investigated the role of atypical @entity14537 ( @entity14537  ) in a myeloid progenitor cell line that expressed @entity17224 (32D.R) and in primary @entity19 bone marrow derived macrophages (BMMs). In 32D.R cells, @entity9827 induced the phosphorylation of @entity14537   and increased its kinase activity. @entity14537 inhibitors and transfections with mutant PKCs showed that optimal @entity9827 -dependent @entity30227 activation and proliferation depended on the activity of @entity14537  . We previously reported that @entity9827 activated the @entity30227 pathway through an @entity56840 -dependent and an @entity56840 independent pathway (Lee and States, Mol. Cell. Biol.18, 6779). @entity14537 inhibitors did not affect @entity9827 induced Ras and @entity56840 activity but markedly reduced @entity13438 and @entity30227 activity, implying that @entity14537   regulated the @entity9827 - @entity30227 pathway at the level of @entity13438 . @entity14537   has been implicated in activating the NF-kB pathway. However, @entity9827 promoted proliferation in an NF-kB independent manner. We established stable 32D.R cell lines that overexpressed @entity14537  . Overexpression of @entity14537   increased the intensity and duration of @entity9827 induced @entity30227 activity and rendered cells more responsive to @entity9827 mediated proliferation. In contrast to 32D.R cells, @entity14537   inhibition in BMMs had only a modest effect on proliferation. Moreover, @entity14537   -specific and pan- @entity14537 inhibitors induced a paradoxical increase in @entity13438 - @entity30227 phosphorylation suggesting that PKCs targeted a common negative regulatory step upstream of @entity13438 . Our results demonstrated that @entity9827 dependent @entity30227 activation and proliferation are regulated differentially in progenitors and differentiated cells.

The role of atypical protein kinase C in @entity9827 -dependent XXXX activation and proliferation in myeloid progenitors and macrophages.

@entity14537 :: ('MESH:D058495', 'Disease') :: ['protein kinase Cs', 'PKC'] @entity9827 :: ('12977(Tax:10090)', 'Gene') :: ['M-CSF', 'CSF-1'] @entity19 :: ('10090', 'Species') :: ['murine'] @entity13438 :: ('17242(Tax:10090)', 'Gene') :: ['MEK'] @entity56840 :: ('11836(Tax:10090)', 'Gene') :: ['A-Raf'] @entity30227 :: ('13844(Tax:10090)', 'Gene') :: ['Erk'] @entity17224 :: ('12978(Tax:10090)', 'Gene') :: ['CSF-1R', 'CSF-1 receptor'] @entity669 :: ('CHEBI:18186', 'Chemical') :: ['tyrosine']
@entity30227 :: (13844(Tax:10090),Gene) :: ['Erk']
