Online now! @thevilchezlab.bsky.social @sedakoyuncu.bsky.social identify age-related hyperactivation of EPS8/RAC signaling in C.elegans as a driver of pathological protein aggregation, highlighting EPS8 and its regulators as potential therapeutic targets.
www.nature.com/articles/s43...
I’d like to thank everyone in the Vilchez Lab @thevilchezlab.bsky.social
and our amazing collaborators Nuria Flames, Yaiza Domínguez Canterla, and Rafael Alis for their enormous help and support throughout this work🙂🥳
Our findings highlight EPS8, RAC, and USP4 as promising targets for future therapies aimed at slowing or preventing disease progression in ALS, Huntington’s disease, and potentially other age-related brain disorders.
By reducing EPS8/RAC activity, we were able to prevent the buildup of toxic protein aggregates and preserve neuronal function in C. elegans models of Huntington’s disease and ALS. Furthermore, we discovered that the deubiquitinating enzyme USP4 regulates EPS8 during aging.
Trilled to share our new work🥳We show that age-related hyperactivation of the EPS8/RAC signaling pathway drives protein aggregation and neurodegeneration — hallmarks of Huntington’s disease and ALS. #proteostasis #aging #neurodegenerativediseases
Happy to have contributed to this exciting work in collaboration with Prof. Dr. Irina Dudanova’s group! If you're interested in learning more about the role of Anle138b in regulating pathological phenotypes in mouse and cellular models of #Huntington’sDisease, check it out!
