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

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Selective requirement for Src kinases during VEGF-induced angiogenesis and vascular permeability.

Src kinase activity was found to protect endothelial cells from apoptosis during vascular endothelial growth factor (VEGF)-, but not basic fibroblast growth factor ( bFGF)-, mediated angiogenesis in chick embryos and mice. In fact, retroviral targeting of kinase-deleted Src to tumor- associated blood vessels suppressed angiogenesis and the growth of a VEGF-producing tumor. Although mice lacking individual Src family kinases (SFKs) showed normal angiogenesis, mice deficient in pp60c-src or pp62c-yes showed no VEGF-induced vascular permeability (VP), yet fyn-/- mice displayed normal VP. In contrast, inflammation-mediated VP appeared normal in Src-deficient mice. Therefore, VEGF-, but not bFGF-, mediated angiogenesis requires SFK activity in general, whereas the VP activity of VEGF specifically depends on the SFKs, Src, or Yes.[1]

References

  1. Selective requirement for Src kinases during VEGF-induced angiogenesis and vascular permeability. Eliceiri, B.P., Paul, R., Schwartzberg, P.L., Hood, J.D., Leng, J., Cheresh, D.A. Mol. Cell (1999) [Pubmed]
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