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pro vyhledávání: '"FUS P525L carrier"'
Publikováno v:
Neurodegenerative diseases
17 (2017): 292–303. doi:10.1159/000480085
info:cnr-pdr/source/autori:Lo Bello M.; Di Fini F.; Notaro A.; Spataro R.; Conforti F.L.; La Bella V./titolo:ALS-Related Mutant FUS Protein Is Mislocalized to Cytoplasm and Is Recruited into Stress Granules of Fibroblasts from Asymptomatic FUS P525L Mutation Carriers/doi:10.1159%2F000480085/rivista:Neurodegenerative diseases (Print)/anno:2017/pagina_da:292/pagina_a:303/intervallo_pagine:292–303/volume:17
17 (2017): 292–303. doi:10.1159/000480085
info:cnr-pdr/source/autori:Lo Bello M.; Di Fini F.; Notaro A.; Spataro R.; Conforti F.L.; La Bella V./titolo:ALS-Related Mutant FUS Protein Is Mislocalized to Cytoplasm and Is Recruited into Stress Granules of Fibroblasts from Asymptomatic FUS P525L Mutation Carriers/doi:10.1159%2F000480085/rivista:Neurodegenerative diseases (Print)/anno:2017/pagina_da:292/pagina_a:303/intervallo_pagine:292–303/volume:17
Background: Amyotrophic lateral sclerosis (ALS) shows a strong genetic basis, with SOD1, FUS, TARDBP, and C9ORF72 being the genes most frequently involved. This has allowed identification of asymptomatic mutation carriers, which may be of help in und
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid_dedup__::6cf5510b2e6d053beedacd94e3075504
http://hdl.handle.net/10447/378861
http://hdl.handle.net/10447/378861