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Article: 'Relax and repair' to restrain aging

Title'Relax and repair' to restrain aging
Authors
KeywordsZmpste24
Senescence
Premature Aging
Prelamin A
Lamin A
Histone Acetylation
Hgps
Epigenetics
Dna Repair
Chromatin
Issue Date2011
PublisherImpact Journals LLC.
Citation
Aging, 2011, v. 3 n. 10, p. 943-954 How to Cite?
AbstractThe maintenance of genomic integrity requires the precise identification and repair of DNA damage. Since DNA is packaged and condensed into higher order chromatin, the events associated with DNA damage recognition and repair are orchestrated within the layers of chromatin. Very similar to transcription, during DNA repair, chromatin remodelling events and histone modifications act in concert to 'open' and relax chromatin structure so that repair proteins can gain access to DNA damage sites. One such histone mark critical for maintaining chromatin structure is acetylated lysine 16 of histone H4 (AcH4K16), a modification that can disrupt higher order chromatin organization and convert it into a more 'relaxed' configuration. We have recently shown that impaired H4K16 acetylation delays the accumulation of repair proteins to double strand break (DSB) sites which results in defective genome maintenance and accelerated aging in a laminopathy-based premature aging mouse model. These results support the idea that epigenetic factors may directly contribute to genomic instability and aging by regulating the efficiency of DSB repair. In this article, the interplay between epigenetic misregulation, defective DNA repair and aging is discussed. © Krishnan et al.
Persistent Identifierhttp://hdl.handle.net/10722/147649
ISSN
2015 Impact Factor: 3.979
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKrishnan, Ven_US
dc.contributor.authorLiu, Ben_US
dc.contributor.authorZhou, Zen_US
dc.date.accessioned2012-05-29T06:05:12Z-
dc.date.available2012-05-29T06:05:12Z-
dc.date.issued2011en_US
dc.identifier.citationAging, 2011, v. 3 n. 10, p. 943-954en_US
dc.identifier.issn1945-4589en_US
dc.identifier.urihttp://hdl.handle.net/10722/147649-
dc.description.abstractThe maintenance of genomic integrity requires the precise identification and repair of DNA damage. Since DNA is packaged and condensed into higher order chromatin, the events associated with DNA damage recognition and repair are orchestrated within the layers of chromatin. Very similar to transcription, during DNA repair, chromatin remodelling events and histone modifications act in concert to 'open' and relax chromatin structure so that repair proteins can gain access to DNA damage sites. One such histone mark critical for maintaining chromatin structure is acetylated lysine 16 of histone H4 (AcH4K16), a modification that can disrupt higher order chromatin organization and convert it into a more 'relaxed' configuration. We have recently shown that impaired H4K16 acetylation delays the accumulation of repair proteins to double strand break (DSB) sites which results in defective genome maintenance and accelerated aging in a laminopathy-based premature aging mouse model. These results support the idea that epigenetic factors may directly contribute to genomic instability and aging by regulating the efficiency of DSB repair. In this article, the interplay between epigenetic misregulation, defective DNA repair and aging is discussed. © Krishnan et al.en_US
dc.languageengen_US
dc.publisherImpact Journals LLC.en_US
dc.relation.ispartofAgingen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectZmpste24en_US
dc.subjectSenescenceen_US
dc.subjectPremature Agingen_US
dc.subjectPrelamin Aen_US
dc.subjectLamin Aen_US
dc.subjectHistone Acetylationen_US
dc.subjectHgpsen_US
dc.subjectEpigeneticsen_US
dc.subjectDna Repairen_US
dc.subjectChromatinen_US
dc.subject.meshAging - genetics-
dc.subject.meshDNA Damage-
dc.subject.meshDNA Repair-
dc.subject.meshNuclear Proteins - chemistry - genetics - metabolism-
dc.subject.meshProtein Precursors - chemistry - genetics - metabolism-
dc.subject.meshAnimals-
dc.subject.meshChromatin - chemistry - metabolism-
dc.subject.meshEpigenesis, Genetic-
dc.subject.meshHistone Deacetylases - metabolism-
dc.subject.meshHistones - metabolism-
dc.subject.meshHumans-
dc.subject.meshLamin Type A - chemistry - genetics - metabolism-
dc.subject.meshMice-
dc.subject.meshProgeria - genetics - physiopathology-
dc.title'Relax and repair' to restrain agingen_US
dc.typeArticleen_US
dc.identifier.emailLiu, B: ppliew@hku.hken_US
dc.identifier.emailZhou, Z: zhongjun@hkucc.hku.hken_US
dc.identifier.authorityLiu, B=rp01485en_US
dc.identifier.authorityZhou, Z=rp00503en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.pmid22067432-
dc.identifier.pmcidPMC3229971-
dc.identifier.scopuseid_2-s2.0-80855144458en_US
dc.identifier.hkuros206819-
dc.identifier.hkuros215051-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80855144458&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume3en_US
dc.identifier.issue10en_US
dc.identifier.spage943en_US
dc.identifier.epage954en_US
dc.identifier.isiWOS:000296799500005-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridZhou, Z=8631856300en_US
dc.identifier.scopusauthoridLiu, B=7408693394en_US
dc.identifier.scopusauthoridKrishnan, V=53363559000en_US

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