CHIP as a therapeutic target for neurological diseases

Carboxy-terminus of Hsc70-interacting protein (CHIP) functions both as a molecular co-chaperone and ubiquitin E3 ligase playing a critical role in modulating the degradation of numerous chaperone-bound proteins. To date, it has been implicated in the regulation of numerous biological functions, incl...

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Published in:Cell death & disease 2020-09, Vol.11 (9), p.727-727, Article 727
Main Authors: Zhang, Shuo, Hu, Zheng-Wei, Mao, Cheng-Yuan, Shi, Chang-He, Xu, Yu-Ming
Format: Article
Language:English
Subjects:
Alzheimer's disease
Animals
Autophagy
Central nervous system
Hemorrhage
Hsc70 protein
Humans
Molecular modelling
Movement disorders
Necroptosis
Nervous System Diseases - therapy
Neurodegenerative diseases
Neurodegenerative Diseases - therapy
Neurological diseases
Parkinson's disease
Pathogenesis
Phagocytosis
Polyglutamine diseases
Protein folding
Review
Therapeutic applications
Trinucleotide repeat diseases
Ubiquitin
Ubiquitin-protein ligase
Ubiquitin-Protein Ligases - pharmacology
Ubiquitin-Protein Ligases - therapeutic use
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Summary:Carboxy-terminus of Hsc70-interacting protein (CHIP) functions both as a molecular co-chaperone and ubiquitin E3 ligase playing a critical role in modulating the degradation of numerous chaperone-bound proteins. To date, it has been implicated in the regulation of numerous biological functions, including misfolded-protein refolding, autophagy, immunity, and necroptosis. Moreover, the ubiquitous expression of CHIP in the central nervous system suggests that it may be implicated in a wide range of functions in neurological diseases. Several recent studies of our laboratory and other groups have highlighted the beneficial role of CHIP in the pathogenesis of several neurological diseases. The objective of this review is to discuss the possible molecular mechanisms that contribute to the pathogenesis of neurological diseases in which CHIP has a pivotal role, such as stroke, intracerebral hemorrhage, Alzheimer's disease, Parkinson's disease, and polyglutamine diseases; furthermore, CHIP mutations could also cause neurodegenerative diseases. Based on the available literature, CHIP overexpression could serve as a promising therapeutic target for several neurological diseases.
ISSN:2041-4889
2041-4889
DOI:10.1038/s41419-020-02953-5