VEGF Induces Tie 2 Shedding via a Phosphoinositide 3-Kinase / Akt – Dependent Pathway to Modulate Tie 2 Signaling
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[1] Siqing Shan,et al. Inhibition of rat corneal angiogenesis by a nuclease-resistant RNA aptamer specific for angiopoietin-2 , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[2] C. Kontos,et al. PTEN Modulates Vascular Endothelial Growth Factor-Mediated Signaling and Angiogenic Effects* , 2002, The Journal of Biological Chemistry.
[3] Y. Fujio,et al. Akt Mediates Cytoprotection of Endothelial Cells by Vascular Endothelial Growth Factor in an Anchorage-dependent Manner* , 1999, The Journal of Biological Chemistry.
[4] J. York,et al. Tyrosine 1101 of Tie2 Is the Major Site of Association of p85 and Is Required for Activation of Phosphatidylinositol 3-Kinase and Akt , 1998, Molecular and Cellular Biology.
[5] P. Rao,et al. Expression of Tie2/Tek in breast tumour vasculature provides a new marker for evaluation of tumour angiogenesis. , 1998, British Journal of Cancer.
[6] G. Nolan,et al. Episomal vectors rapidly and stably produce high-titer recombinant retrovirus. , 1996, Human gene therapy.
[7] P. Rao,et al. GRB2 and SH-PTP2: potentially important endothelial signaling molecules downstream of the TEK/TIE2 receptor tyrosine kinase. , 1995, Oncogene.
[8] D. Dumont,et al. The endothelial-specific receptor tyrosine kinase, tek, is a member of a new subfamily of receptors. , 1993, Oncogene.
[9] E. Jaffe,et al. Culture of human endothelial cells derived from umbilical veins. Identification by morphologic and immunologic criteria. , 1973, The Journal of clinical investigation.