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Article: Aurora kinases and DNA damage response

TitleAurora kinases and DNA damage response
Authors
KeywordsCancer
DNA repair
Cancer therapies
DNA damage checkpoints
Mitosis
Issue Date2020
Citation
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 2020, v. 821, article no. 111716 How to Cite?
AbstractIt is well established that Aurora kinases perform critical functions during mitosis. It has become increasingly clear that the Aurora kinases also perform a myriad of non-mitotic functions including DNA damage response. The available evidence indicates that inhibition Aurora kinase A (AURKA) may contribute to the G2 DNA damage checkpoint through AURKA's functions in PLK1 and CDC25B activation. Both AURKA and Aurora kinase B (AURKB) are also essential in mitotic DNA damage response that guard against DNA damage-induced chromosome segregation errors, including the control of abscission checkpoint and prevention of micronuclei formation. Dysregulation of Aurora kinases can trigger DNA damage in mitosis that is sensed in the subsequent G1 by a p53-dependent postmitotic checkpoint. Aurora kinases are themselves linked to the G1 DNA damage checkpoint through p53 and p73 pathways. Finally, several lines of evidence provide a connection between Aurora kinases and DNA repair and apoptotic pathways. Although more studies are required to provide a comprehensive picture of how cells respond to DNA damage, these findings indicate that both AURKA and AURKB are inextricably linked to pathways guarding against DNA damage. They also provide a rationale to support more detailed studies on the synergism between small-molecule inhibitors against Aurora kinases and DNA-damaging agents in cancer therapies.
Persistent Identifierhttp://hdl.handle.net/10722/307302
ISSN
2022 Impact Factor: 2.3
2023 SCImago Journal Rankings: 0.699
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMa, Hoi Tang-
dc.contributor.authorPoon, Randy Y.C.-
dc.date.accessioned2021-11-03T06:22:20Z-
dc.date.available2021-11-03T06:22:20Z-
dc.date.issued2020-
dc.identifier.citationMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 2020, v. 821, article no. 111716-
dc.identifier.issn0027-5107-
dc.identifier.urihttp://hdl.handle.net/10722/307302-
dc.description.abstractIt is well established that Aurora kinases perform critical functions during mitosis. It has become increasingly clear that the Aurora kinases also perform a myriad of non-mitotic functions including DNA damage response. The available evidence indicates that inhibition Aurora kinase A (AURKA) may contribute to the G2 DNA damage checkpoint through AURKA's functions in PLK1 and CDC25B activation. Both AURKA and Aurora kinase B (AURKB) are also essential in mitotic DNA damage response that guard against DNA damage-induced chromosome segregation errors, including the control of abscission checkpoint and prevention of micronuclei formation. Dysregulation of Aurora kinases can trigger DNA damage in mitosis that is sensed in the subsequent G1 by a p53-dependent postmitotic checkpoint. Aurora kinases are themselves linked to the G1 DNA damage checkpoint through p53 and p73 pathways. Finally, several lines of evidence provide a connection between Aurora kinases and DNA repair and apoptotic pathways. Although more studies are required to provide a comprehensive picture of how cells respond to DNA damage, these findings indicate that both AURKA and AURKB are inextricably linked to pathways guarding against DNA damage. They also provide a rationale to support more detailed studies on the synergism between small-molecule inhibitors against Aurora kinases and DNA-damaging agents in cancer therapies.-
dc.languageeng-
dc.relation.ispartofMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis-
dc.subjectCancer-
dc.subjectDNA repair-
dc.subjectCancer therapies-
dc.subjectDNA damage checkpoints-
dc.subjectMitosis-
dc.titleAurora kinases and DNA damage response-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.mrfmmm.2020.111716-
dc.identifier.pmid32738522-
dc.identifier.scopuseid_2-s2.0-85088667447-
dc.identifier.volume821-
dc.identifier.spagearticle no. 111716-
dc.identifier.epagearticle no. 111716-
dc.identifier.eissn1879-2871-
dc.identifier.isiWOS:000593749300016-

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