Protein-protein interactions reveal key canonical pathways, upstream regulators, interactome domains, and novel targets in ALS.

ABSTRACT: Developing effective treatment strategies for neurodegenerative diseases require an understanding of the underlying cellular pathways that lead to neuronal vulnerability and progressive degeneration. To date, numerous mutations in 147 distinct genes are identified to be "associated" with, "modifier" or "causative" of amyotrophic lateral sclerosis (ALS). Protein products of these genes and their interactions helped determine the protein landscape of ALS, and revealed upstream modulators, key canonical pathways, interactome domains and novel therapeutic targets. Our analysis originates from known human mutations and circles back to human, revealing increased PPARG and PPARGC1A expression in the Betz cells of sALS patients and patients with TDP43 pathology, and emphasizes the importance of li

SUBMITTER: Dervishi I 

PROVIDER: S-EPMC6170493 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature