In:
Current Neuropharmacology, Bentham Science Publishers Ltd., Vol. 19, No. 7 ( 2021-07), p. 1038-1068
Kurzfassung:
Neurodegenerative diseases are characterized by the increasing dysfunction and death of
neurons, resulting in progressive impairment of a person’s mobility and/or cognition. Protein misfolding and aggregation are commonly hypothesized to cause neurotoxicity and, eventually, neuronal
degeneration that are associated with these diseases. Emerging experimental evidence, as well as recent findings from human studies, reveal that the C-terminus of Hsp70 Interacting Protein
(CHIP), or STIP1 Homology and U-box containing Protein 1 (STUB1), is a quality control protein involved in neurodegeneration. Here, we review evidence that CHIP interacts with and plays a role
in regulating proteins implicated in the pathogenesis of Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, and polyglutamine diseases, including Huntington’s disease and
spinocerebellar ataxias. We also review clinical findings identifying mutations in STUB1 as a cause of both autosomal recessive and autosomal dominant forms of cerebellar ataxia. We propose that
CHIP modulation may have therapeutic potential for the treatment of multiple neurodegenerative diseases.
Materialart:
Online-Ressource
ISSN:
1570-159X
DOI:
10.2174/1570159X18666201116145507
Sprache:
Englisch
Verlag:
Bentham Science Publishers Ltd.
Publikationsdatum:
2021
ZDB Id:
2119376-9
