A triskelion of nucleic acids drives protein aggregation in A-T

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 pr...

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Bibliographic Details
Published in:Molecular cell 2021-04, Vol.81 (7), p.1367-1369
Main Authors: Gonzalez-Leal, Claudia, Ladurner, Andreas G.
Format: Article
Language:English
Subjects:
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
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Summary: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. 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.
ISSN:1097-2765
1097-4164
DOI:10.1016/j.molcel.2021.03.017