Publication: Cytoplasmic inclusions of TDP-43 in neurodegenerative
diseases: A potential role for caspases
| dc.contributor.author | Rohn, Troy T. | es |
| dc.date.accessioned | 2013-09-24T11:40:12Z | |
| dc.date.available | 2013-09-24T11:40:12Z | |
| dc.date.issued | 2009 | |
| dc.description.abstract | TAR DNA-binding protein-43 (TDP-43) proteinopathies are classified based upon the extent of modified TDP-43 inclusions and include a growing number of neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), frontotemporal lobar degeneration with ubiquitin immunoreactive, tau negative inclusions (FTLD-U) and FTLD with motor neuron disease (FTLD-MND). In addition, TDP-43 inclusions have also been identified in a number of other neurodegenerative disorders including Alzheimer’s disease, corticobasal degeneration, Lewy body related diseases and Pick’s disease. Current understanding suggests that in these diseases, TDP-43 is relocated from the nucleus to the cytoplasm and sequestered into inclusions that contain modified TDP-43. Major modifications of TDP-43 have been identified as being hyperphosphorylation and proteolytic cleavage by caspases. In this review a summary of the major findings regarding the proteolytic modification of TDP-43 will be discussed as well as potential toxic-gain mechanisms these fragments may cause including cytoskeletal disruptions. | es |
| dc.format | application/pdf | es |
| dc.format.extent | 6 | es |
| dc.identifier.issn | 0213-3911 | es |
| dc.identifier.uri | http://hdl.handle.net/10201/36060 | |
| dc.language | eng | es |
| dc.publisher | Murcia : F. Hernández | es |
| dc.relation.ispartof | Histology and histopathology | es |
| dc.rights | info:eu-repo/semantics/openAccess | es |
| dc.subject | Alzheimer’s disease | es |
| dc.subject | Hirano Bodies | es |
| dc.subject.other | 57 - Biología | es |
| dc.title | Cytoplasmic inclusions of TDP-43 in neurodegenerative diseases: A potential role for caspases | es |
| dc.type | info:eu-repo/semantics/article | es |
| dspace.entity.type | Publication | es |
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