Atg9b Activators

Atg9b Activators encompass a variety of compounds that engage in the upregulation of autophagy, a cellular degradation and recycling process in which Atg9b plays a crucial role. Compounds like Rapamycin, Torin 1, and Metformin act by inhibiting the mTOR pathway or activating AMPK, both of which are upstream signals that lead to the induction of autophagy. Inhibition of mTOR or activation of AMPK results in the de-repression of autophagy-related processes,Atg9b Activators encompass a variety of compounds that engage in the upregulation of autophagy, a cellular degradation and recycling process in which Atg9b plays a crucial role. Compounds like Rapamycin and Metformin act by inhibiting the mTOR pathway or activating AMPK, both of which are upstream signals that lead to the induction of autophagy. Inhibition of mTOR or activation of AMPK results in the de-repression of autophagy-related processes, thus necessitating the trafficking function of Atg9b to supply membrane materials to autophagosomes. Similarly, the induction of autophagy by drugs like Carbamazepine and Lithium, through the inhibition of inositol synthesis and IP3 levels, underlines their role in the enhancement of Atg9b function. Even more, Spermidine and Resveratrol, which act through epigenetic modifications and the activation of SIRT1 respectively, lead to increased autophagic activity. SIRT1-mediated deacetylation of autophagy-related proteins augments autophagy, and in doing so, enhances the requirement for Atg9b's involvement in autophagosomal membrane dynamics.

Additionally, specific compounds like Trehalose, NMN, and Salicylate indirectly promote the activity of Atg9b by initiating or enhancing autophagic flux through distinct mechanisms. Trehalose, through TFEB activation, NMN by boosting NAD+ and SIRT1 activity, and Salicylate via AMPK activation, all lead to an increased functional load on Atg9b to facilitate the formation and trafficking of autophagosomes. Furthermore, Verapamil, which induces autophagy via cytosolic calcium elevation and AMPK activation, and Spautin-1, through inhibition of USP10 and USP13 stabilizing the Beclin1-Vps34 complex, are exemplary in showcasing the indirect activation of Atg9b.