Cyclin F, Neurodegeneration, and the Pathogenesis of ALS/FTD.
| Autor: | Rayner SL; Macquarie Medical School, Macquarie University, Sydney, Australia., Hogan A; Macquarie Medical School, Macquarie University, Sydney, Australia., Davidson JM; Macquarie Medical School, Macquarie University, Sydney, Australia., Cheng F; Macquarie Medical School, Macquarie University, Sydney, Australia., Luu L; Macquarie Medical School, Macquarie University, Sydney, Australia., Morsch M; Macquarie Medical School, Macquarie University, Sydney, Australia., Blair I; Macquarie Medical School, Macquarie University, Sydney, Australia., Chung R; Macquarie Medical School, Macquarie University, Sydney, Australia., Lee A; Macquarie Medical School, Macquarie University, Sydney, Australia. |
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| Jazyk: | angličtina |
| Zdroj: | The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry [Neuroscientist] 2024 Apr; Vol. 30 (2), pp. 214-228. Date of Electronic Publication: 2022 Sep 05. |
| DOI: | 10.1177/10738584221120182 |
| Abstrakt: | Amyotrophic lateral sclerosis (ALS) is the most common form of motor neuron disease and is characterized by the degeneration of upper and lower motor neurons of the brain and spinal cord. ALS is also linked clinically, genetically, and pathologically to a form of dementia known as frontotemporal dementia (FTD). Identifying gene mutations that cause ALS/FTD has provided valuable insight into the disease process. Several ALS/FTD-causing mutations occur within proteins with roles in protein clearance systems. This includes ALS/FTD mutations in CCNF , which encodes the protein cyclin F: a component of a multiprotein E3 ubiquitin ligase that mediates the ubiquitylation of substrates for their timely degradation. In this review, we provide an update on the link between ALS/FTD CCNF mutations and neurodegeneration. Competing Interests: Declaration of Conflicting InterestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. |
| Databáze: | MEDLINE |
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