Forskolin and IBMX, for example, elevate cAMP, subsequently triggering a cascade via protein kinase A that can amplify ABHD15's role in lipid metabolism. Increasing cAMP levels can set off a chain reaction, ultimately reaching ABHD15 and modulating its activity. AMP-activated protein kinase activators like AICAR and 1,1-Dimethylbiguanide, Hydrochloride recalibrate the cell's energy equilibrium, potentially steering ABHD15 activity in a direction that aligns with the altered metabolic demands. By tweaking the energy status of the cell, these activators can create a milieu conducive to enhanced ABHD15 action.
PPAR agonists, including rosiglitazone, pioglitazone, and GW501516, navigate through the genomic labyrinth to fine-tune the expression of genes, possibly nudging ABHD15's expression upward. These agonists exert their influence by regulating lipid metabolism, a domain where ABHD15 is an integral player, thereby setting the stage for its enhanced activity. Nutrient-derived molecules like nicotinamide riboside serve as precursors to NAD+, a coenzyme that participates in redox reactions and may also touch upon sirtuin pathways, potentially implicating ABHD15's function in relation to energy management and lipid processes. Endogenous fatty acid amides such as palmitoylethanolamide and oleoylethanolamide, alongside fatty acids like linoleic acid and alpha-linolenic acid, dive deep into the lipid signaling sea, where they may influence ABHD15's activity by altering the balance and flux of lipid mediators.
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