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CSF1 — EPHB2

Text-mined interactions from Literome

Wilson et al., Biochem J 1999 : Surprisingly, in the light of previous studies with other cells, the PP2A dependent proliferation could be dissociated from activation by extracellular signal regulated protein kinase ( ERK ) in macrophages because OA did not affect either the basal or CSF-1 induced ERK activity in BMM
Lee et al., Oncogene 1999 (Breast Neoplasms) : ERK activation by CSF-1 was robust and sustained in MCF-7fms and to a much lesser extent in T-47Dfms. Using pharmacological and transient transfection approaches, we showed that ERK activation was necessary and sufficient for p21 induction in MCF-7fms
Rovida et al., Oncogene 2002 : ERK activation was increased by MCSF doses capable to elicit a mitogenic response ( 2-5 U/ml ) ... On the contrary, MCSF doses as low as 0.05 U/ml markedly reduced ERK phosphorylation and nuclear content and moderately but significantly reduced cell proliferation
Bhatt et al., J Immunol 2002 : Because M-CSF also induces activation of the mitogen activated protein ( MAP ) kinase extracellular regulated kinase (Erk) , we focused on dissecting the mechanism used by M-CSF to induce Erk activation in human monocytes ... Erk activation by M-CSF also seemed to play a role in cellular survival in monocytes
Jenkins et al., Mol Cell Biol 2004 (MAP Kinase Signaling System) : By contrast, tyrosine phosphorylation of ERK1/2 in response to M-CSF was reduced in gp130 ( Y757F/Y757F ) BMMs, and the pattern of ERK1/2 activation in gp130 mutant BMMs correlated with their opposing responsiveness to M-CSF induced proliferation
Bowdish et al., J Immunol 2004 (MAP Kinase Signaling System) : Activation of ERK1/2 and p38 was markedly increased by the presence of GM-CSF, but not M-CSF
Kwak et al., Biochem Pharmacol 2004 (Bone Resorption) : M-CSF and RANKL activate the ERK , Akt, and NF-kappaB signal transduction pathways, and SCOH suppressed this activation
Gunawardane et al., Cancer Res 2005 (Breast Neoplasms...) : Constitutive activation of the extracellular signal regulated kinase ( ERK ) pathway also enhanced PDEF induced motility and invasion, suggesting that activation of the ERK/mitogen activated protein kinase by ErbB2 and CSF-1R/CSF-1 can cooperate with PDEF to promote motility and invasion
Manes et al., FEBS J 2006 : Overexpression of SLAP-2 in bone marrow macrophages partially suppressed the CSF-1 induced tyrosine phosphorylation and/or expression level of a approximately 80 kDa protein without affecting CSF-1 induced global tyrosine phosphorylation, or activation of Akt or Erk1/2
Sánchez-Tilló et al., J Immunol 2006 : However, whereas ERK phosphorylation in response to M-CSF is Raf-1 dependent, in response to LPS, an alternative pathway directs the activation of these kinases
Wang et al., Am J Respir Cell Mol Biol 2007 : Macrophages from p47 ( phox-/- ) mice, lacking a key component of the NADPH oxidase complex required for ROS generation, had reduced cell survival and Akt1 and p38 mitogen activated protein kinase ( MAPK ) phosphorylation compared with wild-type macrophages in response to M-CSF stimulation, but had no difference in M-CSF stimulated Erk
Suzu et al., J Cell Physiol 2007 : Under the proliferation inducing conditions ( TPA-free ), parental or Nef-inactive cells showed modest ERK activation following M-CSF stimulation, whereas Nef-active cells showed an earlier and transient ERK activation, despite a decrease in their proliferation rate ... Under the differentiation inducing conditions, parental or Nef-inactive cells showed increased and prolonged ERK activation following M-CSF stimulation, whereas Nef-active cells showed transient ERK activation
Bradley et al., J Biol Chem 2008 (MAP Kinase Signaling System) : This study investigates M-CSF mediated MEK/ERK activation and identifies a downstream effector of this pathway ... M-CSF activates MEK/ERK and induces MEK dependent expression of the immediate early gene Egr2
Bradley et al., J Cell Biochem 2008 : While M-CSF mediated MEK/ERK activation promotes osteoclast survival, the signaling pathway by which M-CSF activates MEK/ERK is unresolved
Zhu et al., Cell Mol Immunol 2008 : Western blotting assay revealed that M-CSF activated ERK, JNK and p38 in both mature and immature macrophages, and cAMP inhibited M-CSF induced ERK , JNK and p38 activation in a time dependent manner
Jack et al., Blood 2009 (MAP Kinase Signaling System) : In summary, M-CSF activates ERK more potently than G-CSF, and thereby induces higher levels of c-Fos and phospho-C/EBPalpha ( S21 ), which may directly interact to favor monopoiesis, whereas G-CSF activates signal transducer and activator of transcription 3 and SHP2, potentially shifting the balance to granulopoiesis via gene induction by C/EBPalpha homodimers and via effects of SHP2 on regulators besides ERK
Hie et al., J Nutr Biochem 2011 (Ascorbic Acid Deficiency...) : VC inhibited the M-CSF induced activation of ERK
Zhang et al., Blood 2011 (MAP Kinase Signaling System) : We previously found that G-CSF induces SHP2 tyrosine phosphorylation and that chemical inhibition of SHP1/SHP2 reduces CFU-G and prevents G-CSF but not M-CSF activation of ERK
Nikolic et al., BMC immunology 2011 : M-CSF increased SR-A expression and function, and required the specific activation of p38 MAPK, but not ERK1/2 or JNK
Lee et al., PloS one 2011 (MAP Kinase Signaling System) : The role of atypical protein kinase C in CSF-1 dependent Erk activation and proliferation in myeloid progenitors and macrophages ... PKC inhibitors and transfections with mutant PKCs showed that optimal CSF-1 dependent Erk activation and proliferation depended on the activity of PKC? ... Our results demonstrated that CSF-1 dependent Erk activation and proliferation are regulated differentially in progenitors and differentiated cells
Wilson et al., Biochem Biophys Res Commun 1998 : cAMP enhances CSF-1 induced ERK activity and c-fos mRNA expression via a MEK dependent and Ras independent mechanism in macrophages
Lee et al., Blood 1999 : cAMP dramatically increased ERK activity in the presence of CSF-1 or IL-3