AI Article Synopsis
- Angiogenesis is crucial for both normal bodily functions and disease development, but the intracellular mechanisms controlling it are not well understood.
- Activating the transcription factor Net via Ras phosphorylation plays a significant role in promoting angiogenesis and expressing VEGF, a key factor for blood vessel growth.
- Research shows that reducing Net levels decreases angiogenesis and VEGF expression, indicating that Net can switch from a regulatory role to an activator in response to signals that promote blood vessel formation.
Article Abstract
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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC196465 | PMC |
| http://dx.doi.org/10.1101/gad.272503 | DOI Listing |
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