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Literature summary for 3.4.21.5 extracted from
- Thrombin stimulation of proteoglycan synthesis in vascular smooth muscle is mediated by protease-activated receptor-1 transactivation of the transforming growth factor beta type I receptor (2010), J. Biol. Chem., 285, 26798-26805.
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | - |
- |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| vascular smooth muscle cell | - |
Homo sapiens | - |
General Information
| General Information | Comment | Organism |
|---|---|---|
| physiological function | the G-protein receptor-coupled agonist thrombin signal changes the structure of proteoglycans produced by vascular smooth muscle cells. Thrombin induces Akt activation and mediates proteoglycan synthesis, which is inhibited by TGF-beta receptor ALK V inhibition, which is not due to the release and autocrine/paracrine action of TGF-beta. A blockade of PAR-1 and ALK V inhibits thrombin-stimulated phosphorylation of Smad2. Regulations, overview | Homo sapiens |
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Release 2023.1 (January 2023)
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