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dc.contributor.authorNazio, Francesca
dc.contributor.authorCecconi, Francesco
dc.contributor.authorMaiani, Emiliano
dc.date.accessioned2021-06-02T10:10:12Z
dc.date.available2021-06-02T10:10:12Z
dc.date.issued2018
dc.identifierONIX_20210602_10.5772/intechopen.71404_350
dc.identifier.urihttps://library.oapen.org/handle/20.500.12657/49236
dc.description.abstractCellular plasticity is modulated by protein posttranslational modifications, which act on most intracellular pathways. Ubiquitination is a versatile posttranslational modification (PTM) that influences protein fate, controlling their degradation or modulating their activity and subcellular localization. The ubiquitin proteasome system, UPS, and the autophagic pathway are the main degradative intracellular machineries, which rely on ubiquitination for their activation and/or the selective recycling of proteins and organelles. Recent findings indicate that the cross talk between UPS and autophagy plays a key role in controlling DNA repair pathways. Even being a cytoplasmic process, it is now clear that autophagy can directly impact on the correct activation of DNA repair. Of note, defects on autophagy are related to the impairment of homologous recombination repair and to an increase of the nonhomologous end joining repair activity. These evidences give new insights into the molecular processes underlying the DNA damage response and provide further explanation for the tumorigenesis associated with autophagy impairment. Moreover, these findings introduce new examples of synthetic lethality between autophagy and DNA repair genes and lead to the possible development of target therapies for tumors with defective autophagy.
dc.languageEnglish
dc.subject.classificationbic Book Industry Communication::P Mathematics & science::PS Biology, life sciences::PSB Biochemistry::PSBC Proteins
dc.subject.otherautophagy, DNA repair, ubiquitination, ubiquitin proteasome system, p62
dc.titleChapter The Cross Talk among Autophagy, Ubiquitination, and DNA Repair: An Overview
dc.typechapter
oapen.identifier.doi10.5772/intechopen.71404
oapen.relation.isPublishedBy09f6769d-48ed-467d-b150-4cf2680656a1
oapen.relation.isFundedByH2020-MSCA-ITN-2014
oapen.grant.number642295
oapen.grant.acronymMEL-PLEX


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