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Modulating rapamycin target protein promotes autophagy, lowering toxic Huntingtin protein

Recent failed clinical trials of a drug designed to clear the mutant Huntingtin protein that causes Huntington s disease (HD) heightens the need for new approaches for the devastating, incurable, progressive neurodegenerative genetic disorder. Scientists at the Buck Institute have found that the targeting the protein called FK506-binding protein 51 or FKBP51 promotes the clearing of those toxic proteins via autophagy, a natural process whereby cells recycle damaged proteins and mitochondria and use them for nutrition. ....

Jesse Simons , Swati Naphade , Michellee Ehrlich , Ningzhe Zhang , Kuruwitage Lakshika Madushani , Stephen Scheeler , Feliz Hausch , Technische Universitat Darmstadt , Kathrineh Schreiber , Jordi Creus Muncunill , Felix Hausch , Mariaa Sanchez , Alejandro Lopez Ramirez , Barbara Bailus , Brian Kennedy , Lisa Ellerby , Stanislav Moroz , Ashley Loureiro , Pioneer Grant Fund , Department Of Neurology , National Institutes Of Health , Other Buck Institute , Buck Institute Doublex Fellowship , Icahn School Of Medicine At Mount Sinai , Technical University In Darmstadt , Buck Institute Ellerby ,