Gene interactions and pathways from curated databases and text-mining

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CSF1 — HSPG2

Text-mined interactions from Literome

Nakamura et al., J Cell Biol 2001 : Furthermore, in Src ( -/- ) pOCs M-CSF , together with filamentous actin, causes recruitment of beta ( 3 ) integrin and PLC-gamma to adhesion contacts and induces stable association of beta ( 3 ) integrin with PLC-gamma , phosphatidylinositol 3-kinase, and PYK2 ... Moreover, direct interaction of PYK2 and PLC-gamma can be induced by either adhesion or M-CSF , suggesting that this interaction may enable the formation of integrin associated complexes
Kertész et al., Eur J Clin Invest 2012 (Bone Resorption...) : PLC?2 was phosphorylated in a Src-family dependent manner upon macrophage adhesion but not upon stimulation by M-CSF or RANKL
Tai et al., Blood 2012 (Multiple Myeloma...) : PCI-32765 blocked RANKL/M-CSF induced phosphorylation of Btk and downstream PLC-?2 in OCs, resulting in diminished TRAP5b ( ED50 = 17 nM ) and bone resorption activity
Downing et al., EMBO J 1989 : Pre-treatment of cells with orthovanadate also led to tyrosine phosphorylation of PLC-gamma which was significantly enhanced by PDGF, but not by CSF-1
Chen et al., Exp Hematol 1993 : The loss of M-CSF receptors induced by LPS can be inhibited by neomycin and compound 48/80, two potent phospholipase C (PLC) inhibitors, but not by phospholipase A2, calpain, protein kinase C ( PKC ) or protease inhibitors ... Our results show that 1 ) TPA induced M-CSF receptor loss is strictly dependent on PKC activation ; 2 ) PLC activation alone also leads to downregulation of M-CSF receptors ; and 3 ) LPS induced M-CSF receptor downregulation in PEM is mediated primarily through a PLC dependent pathway