Metabolism
Serine/threonine kinase AMPK upregulates glucose uptake by promoting the expression and function of glucose transporters. AMPK is activated by increased AMP/ATP ratio, resulting from cellular and environmental stress, e.g. low glucose, heat shock, hypoxia and ischemia. AMPK activation positively modulates signaling transductions that refill ATP levels. Moreover, it also stimulates catabolic processes such as fatty acid oxidation and glycolysis through inhibition of ACC and activation of PFK2. AMPK negatively regulates various proteins which are important to ATP-consuming mechanisms, e.g. mTORC2, glycogen synthase, SREBP-1, and TSC2, causing the downregulation/inhibition of gluconeogenesis and glycogen, lipid and protein synthesis.
- B3703 LB42708Target: FtaseSummary: Selective FTase inhibitor
- B4669 VidofludimusSummary: DHODH inhibitor
- B6273 (±)-Acetylcarnitine chlorideSummary: weak cholinergic agonist; intermediates in lipid metabolism
- B6294 Ro 20-1724Summary: PDE4 inhibitor
- B6315 (±)-Decanoylcarnitine chlorideSummary: intermediate in lipid metabolism
- B6354 (±)-Myristoylcarnitine chlorideSummary: cholinergic agonist; important intermediates in lipid metabolism
- B6371 (±)-Octanoylcarnitine chloride5 CitationSummary: an intermediate in fatty acid metabolism
- B6375 (±)-Propionylcarnitine chlorideSummary: homolog of acetylcarnitine chloride
- B6747 PACOCF3Summary: CPLA2 and iPLA2 inhibitor
- B6893 m-3M3FBSSummary: PLC activator