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Nucleocytoplasmic transport inC9orf72-mediated ALS/FTD
| Content Provider | Scilit |
|---|---|
| Author | Zhang, Ke Grima, Jonathan C. Rothstein, Jeffery D. Lloyd, Thomas E. |
| Copyright Year | 2016 |
| Description | A GGGGCC hexanucleotide repeat expansion in C9orf72 is the most common genetic cause of familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Recent studies indicate that disruption of nucleocytoplasmic transport pathways play a critical role in the pathogenesis of C9orf72-mediated ALS/FTD (C9-ALS). Here, we discuss mechanisms by which C9orf72 mutations cause nucleocytoplasmic transport deficits and contribute to disease pathogenesis. We review the current literature regarding nucleocytoplasmic transport disruption in C9-ALS, and discuss implications and directions for future research. |
| Related Links | https://www.tandfonline.com/doi/pdf/10.1080/19491034.2016.1172152?needAccess=true https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916865/pdf |
| Ending Page | 137 |
| Page Count | 6 |
| Starting Page | 132 |
| ISSN | 19491034 |
| e-ISSN | 19491042 |
| DOI | 10.1080/19491034.2016.1172152 |
| Journal | Nucleus |
| Issue Number | 2 |
| Volume Number | 7 |
| Language | English |
| Publisher | Informa UK Limited |
| Publisher Date | 2016-03-01 |
| Access Restriction | Open |
| Subject Keyword | Journal: Nucleus Neurosciences Amyotrophic Lateral Sclerosis (als) C9orf72 Frontotemporal Dementia (ftd) Hexanucleotide Repeat Expansion (hre) Nucleocytoplasmic Transport Nuclear Pore Complex (npc) Ran Gtpase |
| Content Type | Text |
| Subject | Cell Biology Medicine |
