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

Gonzalez-Leal, Claudia; Ladurner, Andreas G

Gonzalez-Leal, Claudia; Ladurner, Andreas G.

Afiliación

Gonzalez-Leal C; Department of Physiological Chemistry, Biomedical Center, Faculty of Medicine, LMU Munich, 82152 Planegg-Martinsried, Germany; International Max Planck Research School for Molecular Life Sciences, 82152 Planegg-Martinsried, Germany.
Ladurner AG; Department of Physiological Chemistry, Biomedical Center, Faculty of Medicine, LMU Munich, 82152 Planegg-Martinsried, Germany; International Max Planck Research School for Molecular Life Sciences, 82152 Planegg-Martinsried, Germany; Eisbach Bio GmbH, Am Klopferspitz 19, 82152 Planegg-Martinsried, Germany. Electronic address: andreas.ladurner@bmc.med.lmu.de.

Mol Cell ; 81(7): 1367-1369, 2021 04 01.

Article en En | MEDLINE | ID: mdl-33798413

ABSTRACT

ABSTRACT

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.

Asunto(s)

Ataxia Telangiectasia; Ácidos Nucleicos; Proteínas de la Ataxia Telangiectasia Mutada; Proteínas de Ciclo Celular/metabolismo; Proteínas de Unión al ADN/metabolismo; Humanos; Poli(ADP-Ribosa) Polimerasa-1; Poli ADP Ribosilación; Poli(ADP-Ribosa) Polimerasas/metabolismo; Agregado de Proteínas; Proteostasis; Proteínas Supresoras de Tumor/genética

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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Ataxia Telangiectasia / Ácidos Nucleicos Límite: Humans Idioma: En Revista: Mol Cell Asunto de la revista: BIOLOGIA MOLECULAR Año: 2021 Tipo del documento: Article País de afiliación: Alemania

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