Hsp70 in Redox Homeostasis.
Hsp70
ROS
cysteine modifications
glutathionylation
oxidative stress
redox homeostasis
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
28 02 2022
28 02 2022
Historique:
received:
19
01
2022
revised:
13
02
2022
accepted:
14
02
2022
entrez:
10
3
2022
pubmed:
11
3
2022
medline:
12
4
2022
Statut:
epublish
Résumé
Cellular redox homeostasis is precisely balanced by generation and elimination of reactive oxygen species (ROS). ROS are not only capable of causing oxidation of proteins, lipids and DNA to damage cells but can also act as signaling molecules to modulate transcription factors and epigenetic pathways that determine cell survival and death. Hsp70 proteins are central hubs for proteostasis and are important factors to ameliorate damage from different kinds of stress including oxidative stress. Hsp70 members often participate in different cellular signaling pathways via their clients and cochaperones. ROS can directly cause oxidative cysteine modifications of Hsp70 members to alter their structure and chaperone activity, resulting in changes in the interactions between Hsp70 and their clients or cochaperones, which can then transfer redox signals to Hsp70-related signaling pathways. On the other hand, ROS also activate some redox-related signaling pathways to indirectly modulate Hsp70 activity and expression. Post-translational modifications including phosphorylation together with elevated Hsp70 expression can expand the capacity of Hsp70 to deal with ROS-damaged proteins and support antioxidant enzymes. Knowledge about the response and role of Hsp70 in redox homeostasis will facilitate our understanding of the cellular knock-on effects of inhibitors targeting Hsp70 and the mechanisms of redox-related diseases and aging.
Identifiants
pubmed: 35269451
pii: cells11050829
doi: 10.3390/cells11050829
pmc: PMC8909019
pii:
doi:
Substances chimiques
HSP70 Heat-Shock Proteins
0
Reactive Oxygen Species
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Ministry of Science and Technology of the People's Republic of China
ID : 2017YFA0504000
Organisme : National Natural Science Foundation of China
ID : 31920103011
Organisme : National Natural Science Foundation of China
ID : 31770829
Organisme : National Natural Science Foundation of China
ID : 32171443
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