A triskelion of nucleic acids drives protein aggregation in A-T.
Ataxia Telangiectasia
Ataxia Telangiectasia Mutated Proteins
Cell Cycle Proteins
/ metabolism
DNA-Binding Proteins
/ metabolism
Humans
Nucleic Acids
Poly (ADP-Ribose) Polymerase-1
Poly ADP Ribosylation
Poly(ADP-ribose) Polymerases
/ metabolism
Protein Aggregates
Proteostasis
Tumor Suppressor Proteins
/ genetics
Journal
Molecular cell
ISSN: 1097-4164
Titre abrégé: Mol Cell
Pays: United States
ID NLM: 9802571
Informations de publication
Date de publication:
01 04 2021
01 04 2021
Historique:
entrez:
2
4
2021
pubmed:
3
4
2021
medline:
10
4
2021
Statut:
ppublish
Résumé
Mutations in ataxia telangiectasia mutated (ATM) kinase lead to cerebellar neurodegeneration. In this issue of Molecular Cell, Lee et al. (2021) revealed how transcription-induced reactive oxygen species and DNA-RNA hybrids activate PARP enzymes, generating the nucleic acid poly-ADP-ribose, which promotes the accumulation of protein aggregates in A-T-like disorders.
Identifiants
pubmed: 33798413
pii: S1097-2765(21)00212-4
doi: 10.1016/j.molcel.2021.03.017
pii:
doi:
Substances chimiques
Cell Cycle Proteins
0
DNA-Binding Proteins
0
Nucleic Acids
0
Protein Aggregates
0
Tumor Suppressor Proteins
0
Poly (ADP-Ribose) Polymerase-1
EC 2.4.2.30
Poly(ADP-ribose) Polymerases
EC 2.4.2.30
ATM protein, human
EC 2.7.11.1
Ataxia Telangiectasia Mutated Proteins
EC 2.7.11.1
Types de publication
Journal Article
Comment
Langues
eng
Sous-ensembles de citation
IM
Pagination
1367-1369Commentaires et corrections
Type : CommentOn
Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests A.G.L. is a co-founder, shareholder, and managing director of Eisbach Bio, a biotech developing small-molecule inhibitors targeting helicases.