The transcription factor Net regulates the angiogenic switch
Autor: | Nicolas Wernert, Marie-Christine Multon, Hong Zheng, Bohdan Wasylyk, Sauveur-Michel Maira, Joseph Abecassis, Abdelkader Ayadi, Jack A. Schalken, Christine Wasylyk, Hermann Rogatsch |
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Rok vydání: | 2003 |
Předmět: |
Male
Vascular Endothelial Growth Factor A Angiogenic Switch Angiogenesis Neovascularization Physiologic Endothelial Growth Factors Biology Neovascularization chemistry.chemical_compound Mice Vasculogenesis Genetics medicine Animals Promoter Regions Genetic Transcription factor Oncogene Proteins Lymphokines Wound Healing Neovascularization Pathologic Proto-Oncogene Proteins c-ets Vascular Endothelial Growth Factors Research Papers Vascular endothelial growth factor Tumor microenvironment [UMCN 1.3] Vascular endothelial growth factor A chemistry Cancer research ras Proteins Intercellular Signaling Peptides and Proteins medicine.symptom Ex vivo Developmental Biology Transcription Factors |
Zdroj: | Genes & Development, 17, 18, pp. 2283-97 Genes & Development, 17, 2283-97 |
ISSN: | 0890-9369 |
Popis: | Item does not contain fulltext Angiogenesis is fundamental to physiological and pathological processes. Despite intensive efforts, little is known about the intracellular circuits that regulate angiogenesis. The transcription factor Net is activated by phosphorylation induced by Ras, an indirect regulator of angiogenesis. Net is expressed at sites of vasculogenesis and angiogenesis during early mouse development, suggesting that it could have a role in blood vessel formation. We show here that down-regulation of Net inhibits angiogenesis and vascular endothelial growth factor (VEGF) expression in vivo, ex vivo, and in vitro. Ras-activated phosphorylated Net (P-Net) stimulates the mouse VEGF promoter through the -80 to -53 region that principally binds Sp1. P-Net and VEGF are coexpressed in angiogenic processes in wild-type mouse tissues and in human tumors. We conclude that Net is a regulator of angiogenesis that can switch to an activator following induction by pro-angiogenic molecules. |
Databáze: | OpenAIRE |
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