Proliferin induces endothelial cell chemotaxis through a G protein-coupled, mitogen-activated protein kinase-dependent pathway.

@article{Groskopf1997ProliferinIE,
  title={Proliferin induces endothelial cell chemotaxis through a G protein-coupled, mitogen-activated protein kinase-dependent pathway.},
  author={J C Groskopf and L J Syu and Alan R. Saltiel and Daniel I. H. Linzer},
  journal={Endocrinology},
  year={1997},
  volume={138 7},
  pages={
          2835-40
        }
}
To investigate the mechanism of action of the placental angiogenic hormone proliferin (PLF), we analyzed the signaling components in endothelial cells that are required for PLF-induced chemotaxis. Pertussis toxin, which inactivates Gi proteins, inhibited PLF-induced chemotaxis of endothelial cells. Gi proteins can lead to activation of the mitogen-activated protein kinase (MAPK) pathway; PLF was found to stimulate MAPK activity, and this induction was blocked by both pertussis toxin and a… CONTINUE READING
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Requirement for the insulin - like growth factor II / mannose 6 - phosphate receptor in proliferin - induced angiogenesis

  • O Volpert, D Jackson, N Bouck, Linzer DIH
  • Endocrinology
  • 1996

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