Chapter 7 Ubiquitinopathies
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In neurological disease and aging, modified proteins are the histopathological hallmarks of a number of diseases, such as SOD1 in amyotrophic lateral sclerosis (ALS), and a class of diseases long referred to as the proteinopathies, including tauopathies in Alzheimer's disease and inclusions of amyloid beta, alpha-synuclein in Parkinson's and multiple secondary ubiquitinopathies.
“In neurological disease and aging, modified proteins are the histopathological hallmarks of a number of diseases, such as SOD1 in amyotrophic lateral sclerosis (ALS) 56,57 , and a class of diseases long referred to as the proteinopathies 57 , including tauopathies in Alzheimer's disease 58 and inclusions of amyloidβ 59 , α -synuclein in Parkinson's 60,61 and multiple secondary ubiquitinopathies”
From How many human proteoforms are there? (2018) · cites this paper as [62]
Cites
Mutations in the endosomal ESCRTIII-complex subunit CHMP2B in frontotemporal dementia
Skibinski, G., Parkinson, N. J., Brown, J. M., Chakrabarti, L., Lloyd, S. L., Hummerich, H., Nielsen, J. E., Hodges, J. R., Spillantini, M. G., Thusgaard, T., et al. (2005) · Nature Genetics · doi:10.1038/ng1609 · Cited by 822 · see citing works
CHIP and Hsp70 regulate tau ubiquitination, degradation and aggregation
Petrucelli, L. (2004) · Human Molecular Genetics · doi:10.1093/hmg/ddh083 · Cited by 735 · see citing works
Braak, H., Braak, E., Grundke-Iqbal, I., & Iqbal, K. (1986) · Neuroscience Letters · doi:10.1016/0304-3940(86)90288-0 · Cited by 432 · see citing works
Arima, K., Uéda, K., Sunohara, N., Arakawa, K., Hirai, S., Nakamura, M., Tonozuka-Uehara, H., & Kawai, M. (1998) · Acta Neuropathologica · doi:10.1007/s004010050917 · Cited by 239 · see citing works
Mutant valosin‐containing protein causes a novel type of frontotemporal dementia
Schröder, R., Watts, G. D. J., Mehta, S. G., Evert, B. O., Broich, P., Fließbach, K., Pauls, K., Hans, V. H., Kimonis, V., & Thal, D. R. (2005) · Annals of Neurology · doi:10.1002/ana.20407 · Cited by 177 · see citing works
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How many human proteoforms are there?
Aebersold, R., Agar, J. N., Amster, I. J., Baker, M. S., Bertozzi, C. R., Boja, E. S., Costello, C. E., Cravatt, B. F., Fenselau, C., Garcia, B. A., et al. (2018) · Nature Chemical Biology · doi:10.1038/nchembio.2576 · Cited by 907 · see citing works
- Authors
- Dickson, D. W.
- Corresponding author
- Dickson, Dennis W.
- ORCID
- Dickson, Dennis W.
- Venue
- Blue Books of Neurology
- Publisher
- Elsevier
- Published
- 2007
- Pages
- 165-185
- ISSN
- 1877-1831 (ISSN-L)
- 1877-184X
- OpenAlex
- W1498802183
- Cited by
- 3
- References
- 5
- Citations by year
- 2020: 1 · 2018: 1 · 2017: 1
- FWCI
- 0.00
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Blue books of neurology (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Keywords
- neurodegeneration, frontotemporal lobar degeneration, motor neuron disease, amyotrophic lateral sclerosis, Alzheimer's disease, protein aggregation, inclusion bodies, ubiquitin conjugation, aging, neurofibrillary tangles, Bunina bodies, granulovacuolar degeneration
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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