Date published: 2025-10-13

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METTL7A Activators

METTL7A Activators are a distinct set of chemical compounds that facilitate the enhancement of METTL7A's functional activity through intricate biochemical pathways. Forskolin and IBMX, through their actions on increasing intracellular cAMP, indirectly promote METTL7A's activity by stimulating protein kinase A (PKA), which may phosphorylate and activate proteins that associate with METTL7A. Similarly, Epigallocatechin gallate (EGCG), by inhibiting various kinases, alleviates constraints on METTL7A's functional pathways, potentially allowing for its increased activity. Phorbol 12-myristate 13-acetate (PMA) directly activates protein kinase C (PKC), which could lead to activation of signaling events that enhance the activity of METTL7A, particularly in the context of its involvement in lipid metabolism.

Further influencing METTL7A's functional landscape, compounds like Sphingosine-1-phosphate and A23187 (Calcimycin) modulate lipid and calciumno info signaling, respectively, creating a conducive environment for the enhancement of METTL7A activity. LY294002 and Wortmannin, as PI3K inhibitors, as well as U0126 and SB203580, which are inhibitors of MEK1/2 and p38 MAPK, respectively, reconfigure the signaling milieu to favor METTL7A's pathway over competing ones. This reconfiguration allows METTL7A to be more functionally active within its role in cellular processes. Genistein's inhibition of tyrosine kinases also plays a part by reducing competitive signaling, thereby indirectly facilitating the enhancement of METTL7A's activity. Lastly, Rolipram, by selectively inhibiting phosphodiesterase 4, raises cAMP levels, which can further support METTL7A activation through PKA-mediated phosphorylation events, emphasizing the complex interplay of intracellular signaling in regulating METTL7A. Collectively, these activators work through a network of signaling pathways to increase the functional activity of METTL7A, underscoring the intricate regulation of its role in cellular metabolism.

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