| First Author | Eliceiri BP | Year | 1999 |
| Journal | Mol Cell | Volume | 4 |
| Issue | 6 | Pages | 915-24 |
| PubMed ID | 10635317 | Mgi Jnum | J:59158 |
| Mgi Id | MGI:1351097 | Doi | 10.1016/s1097-2765(00)80221-x |
| Citation | Eliceiri BP, et al. (1999) Selective requirement for Src kinases during VEGF-induced angiogenesis and vascular permeability. Mol Cell 4(6):915-24 |
| abstractText | 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. |
