The designation SDSL Activators encompasses a diverse array of compounds that can influence the activity of SDSL through modulation of various metabolic pathways. Compounds such as A-769662 and AICAR function as activators of AMP-activated protein kinase, a central regulator of cellular energy homeostasis, which in turn can augment the demand for SDSL function in lipid metabolism. Agonists of PPAR isoforms like GW501516, pioglitazone, fenofibrate, and OEA act on nuclear receptors that directly regulate the expression of genes involved in lipid synthesis and degradation, potentially necessitating enhanced SDSL activity to meet the altered metabolic requirements.
Other compounds, such as GW3965 and SRT1720, engage with liver X receptors and sirtuin pathways, respectively, modulating the expression of numerous genes, including those involved in lipid homeostasis, which may lead to increased SDSL activity. Pioglitazone and fenofibrate, through their actions on PPARγ and PPARα, orchestrate a wide array of lipid metabolic processes that can indirectly necessitate the activation of SDSL. Furthermore, molecules like 4-Phenylbutyrate and nicotinamide riboside can induce changes in gene expression and NAD+ metabolism, respectively, thereby influencing the activity of SDSL. Choline, an essential nutrient, plays a pivotal role in lipid metabolism, and its availability can impact the function of lipid-metabolizing enzymes, including SDSL.
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