The abstract states that both proteasomal and autophagic pathways degrade mutant Htt, with CMA being one option, but doesn't explain the molecular switches that direct substrates to specific degradation routes. Understanding pathway selection could enable targeted therapeutic manipulation. Gap type: unexplained_observation Source paper: Role of chaperone-mediated autophagy in degrading Huntington's disease-associated huntingtin protein. (2014, Acta biochimica et biophysica Sinica, PMID:24323530)
Landscape Summary: What determines whether mutant huntingtin is degraded by CMA versus other autophagy pathways? is a 0.8 priority gap in neurodegeneration. It has 0 linked hypotheses with average composite score 0.000. Status: open.
Colonna, Sevlever, et al. (TREM2 biology)
What determines whether mutant huntingtin is degraded by CMA versus other autophagy pathways? — INVOKE-2 (completed)
No hypotheses linked to this gap yet.
No activity recorded yet.
No discussions yet. Be the first to comment.
Create sub-tasks to investigate specific aspects of this gap: