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CSF3 — EPHB2

Text-mined interactions from Literome

Iida et al., Leukemia 1999 (Acute Disease...) : Three samples with N-Ras mutations were stimulated with IL-3, GM-CSF and G-CSF separately but ERK2 activation was induced in none of these samples stimulated with these cytokines
Dong et al., J Biol Chem 2001 (MAP Kinase Signaling System) : Granulocyte colony stimulating factor induces ERK5 activation, which is differentially regulated by protein-tyrosine kinases and protein kinase C. Regulation of cell proliferation and survival ... Different from other members of the MAPK family including Erk1/2, JNK, and p38, maximal activation of Erk5 by G-CSF required the C-terminal region of the G-CSF receptor ... Genistein, a specific inhibitor of protein-tyrosine kinases, blocked G-CSF induced Erk5 activation ... In contrast, inhibition of protein kinase C activity increased G-CSF mediated activation of Erk5 and MEK5, whereas stimulation of protein kinase C activity inhibited activation of the two kinases by G-CSF
Srinivasa et al., Leukemia 2002 (Leukemia, Monocytic, Acute...) : These data suggest that OCI-AML5 cells proliferate at least in part, due to the activation of both ERK and p38 MAP kinase pathways in response to G-CSF and FL
Kutsuna et al., Am J Physiol Cell Physiol 2004 : These findings suggest that TNF, GM-CSF, and G-CSF induce actin depolymerization and morphological changes through activation of ERK and/or p38 MAPK and that cytokine induced actin reorganization may be partly responsible for the inhibitory effect of these cytokines on neutrophil chemotaxis
Nishiki et al., Am J Physiol Cell Physiol 2004 (MAP Kinase Signaling System) : G-CSF did not affect LPS induced activation of ERK , p38, JNK, and NF-kappa B, indicating that G-CSF affects the pathway downstream or independently of these signaling molecules
Murata-Ohsawa et al., Int J Mol Med 2004 (Leukemia, Myeloid...) : Pre-exposure to Delta-1 did not affect the phosphorylation of ERK1/2 and STAT3 induced by G-CSF in OCI/AML-6 cells, either
Kamezaki et al., Stem Cells 2005 : Roles of Stat3 and ERK in G-CSF signaling ... Stat3-null bone marrow cells displayed a significant activation of extra-cellular regulated kinase 1 (ERK1)/ERK2 under basal conditions, and the activation of ERK was enhanced and sustained by G-CSF stimulation
Miranda et al., Leuk Res 2005 (MAP Kinase Signaling System) : Additionally, interleukin-3, which inhibits G-CSF induced differentiation of 32 Dc l3 cells, also inhibited the ability of G-CSF to stimulate prolonged MEK/ERK activation
Yagyu et al., Int J Cancer 2006 (Carcinoma, Lewis Lung...) : Here, we show that 1 ) higher frequency of spontaneous 3LL lung metastasis was observed in Bik-/- mice compared to Bik+/+ mice, suggesting that bikunin deficiency increases the sensitivity of mice to lung metastasis ; 2 ) administration of exogenous bikunin caused a significant reduction of lung metastasis in Bik-/- and Bik+/+ mice ; 3 ) primary and metastatic tumors significantly upregulated uPA and PAI-1 expression in Bik-/- mice relative to Bik+/+ mice at least through phosphorylation of ERK1/2 and 4 ) exogenous bikunin suppressed phosphorylation of ERK1/2 and upregulation of uPA and PAI-1 expression in 3LL cells in response to G-CSF
Nakamae-Akahori et al., Immunology 2006 : These findings are consistent with the fact that G-CSF selectively activates MEK/ERK and PI3K, but not p38, in neutrophils
Kamio et al., Mol Cell Endocrinol 2008 (Inflammation...) : Collectively, these results suggest that MEK1/2-ERK1/2 signaling is involved in the adiponectin induced secretion of G-CSF
Lee et al., Oncol Rep 2013 : Therefore, ERK2 ( but not ERK1 ) is responsible for the transcriptional regulation of tumor derived G-CSF
Suzuki et al., Blood 1999 : MEK inhibitor ( PD98059 ) reduced tyrosine phosphorylation of ERK , but not p38 MAPK, induced by G-CSF , GM-CSF, or TNF