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A:
It's easy to create a.vbs file for one-off use that can do this for you. If you look at the documentation, you'll see that the parameter you're looking for is olApp.Activate.
Endothelin-1 stimulates angiogenesis through the activation of mitogen-activated protein kinases in endothelial cells.
Endothelium is a dynamic endocrine organ that plays an important role in cardiovascular homeostasis and disease. Stimulation of endothelial cells by several molecules of the vasoactive peptide family induces angiogenesis, the formation of new blood vessels. We have characterized the intracellular signaling mechanisms triggered by endothelin-1, a potent vasoconstrictor and mitogen for endothelial cells, which results in the stimulation of angiogenesis. The mitogen-activated protein kinase (MAPK) activation induced by endothelin-1 is a complex response that involves sequential activation of MAPK/extracellular signal-regulated kinase (ERK) 1 and MAPK/ERK2. The transient activation of MAPK/ERK1 and MAPK/ERK2 by endothelin-1 is mediated by the differential activation of phosphatidylinositol 3-kinase (PI3K). In contrast, endothelin-1 stimulates the sustained activation of MAPK/ERK2 via the activation of a distinct PI3K activity. Inhibition of endothelin-1-induced activation of MAPK/ERK1 and MAPK/ERK2 blocks endothelin-1-mediated angiogenesis, indicating that activation of ERKs is required for the angiogenic action of endothelin-1. Endothelin-1-induced angiogenesis is also suppressed by the inhibition of both MAPK/ERK1 and MAPK/ERK2, indicating a synergistic role for the two MAPK pathways. Collectively, our results identify a PI3K-dependent pathway that mediates the activation of ERKs by endothelin-1, and they support a critical role for MAPK signaling in angiogenesis.Starting with the first release back in 2003 (R4), we have been trying to automate this for the last 8 years.
That’s what we do best: automate.
With your help we can finally release the version that has been on the drawing board for years
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