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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

16K human prolactin inhibits vascular endothelial growth factor-induced activation of Ras in capillary endothelial cells.

Signaling pathways mediating the antiangiogenic action of 16K human (h)PRL include inhibition of vascular endothelial growth factor (VEGF)-induced activation of the mitogen-activated protein kinases ( MAPK). To determine at which step 16K hPRL acts to inhibit VEGF- induced MAPK activation, we assessed more proximal events in the signaling cascade. 16K hPRL treatment blocked VEGF- induced Raf-1 activation as well as its translocation to the plasma membrane. 16K hPRL indirectly increased cAMP levels; however, the blockade of Raf-1 activation was not dependent on the stimulation of cAMP-dependent protein kinase (PKA), but rather on the inhibition of the GTP-bound Ras. The VEGF- induced tyrosine phosphorylation of the VEGF receptor, Flk-1, and its association with the Shc/Grb2/Ras-GAP (guanosine triphosphatase- activating protein) complex were unaffected by 16K hPRL treatment. In contrast, 16K hPRL prevented the VEGF- induced phosphorylation and dissociation of Sos from Grb2 at 5 min, consistent with inhibition by 16K hPRL of the MEK/ MAPK feedback on Sos. The inhibition of Ras activation was paralleled by the increased phosphorylation of 120 kDa proteins comigrating with Ras-GAP. Taken together, these findings show that 16K hPRL inhibits the VEGF-induced Ras activation; this antagonism represents a novel and potentially important mechanism for the control of angiogenesis.[1]

References

  1. 16K human prolactin inhibits vascular endothelial growth factor-induced activation of Ras in capillary endothelial cells. D'Angelo, G., Martini, J.F., Iiri, T., Fantl, W.J., Martial, J., Weiner, R.I. Mol. Endocrinol. (1999) [Pubmed]
 
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