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Article: Distinct versus overlapping functions of MDC1 and 53BP1 in DNA damage response and tumorigenesis

TitleDistinct versus overlapping functions of MDC1 and 53BP1 in DNA damage response and tumorigenesis
Authors
KeywordsSpecies Index: Ataxia Telangiectasia
Mus
Issue Date2008
PublisherRockefeller University Press. The Journal's web site is located at http://www.jcb.org
Citation
Journal Of Cell Biology, 2008, v. 181 n. 5, p. 727-735 How to Cite?
AbstractThe importance of the DNA damage response (DDR) pathway in development, genomic stability, and tumor suppression is well recognized. Although 53BP1 and MDC1 have been recently identified as critical upstream mediators in the cellular response to DNA double-strand breaks, their relative hierarchy in the ataxia telangiectasia mutated (ATM) signaling cascade remains controversial. To investigate the divergent and potentially overlapping functions of MDC1 and 53BP1 in the ATM response pathway, we generated mice deficient for both genes. Unexpectedly, the loss of both MDC1 and 53BP1 neither significantly increases the severity of defects in DDR nor increases tumor incidence compared with the loss of MDC1 alone. We additionally show that MDC1 regulates 53BP1 foci formation and phosphorylation in response to DNA damage. These results suggest that MDC1 functions as an upstream regulator of 53BP1 in the DDR pathway and in tumor suppression. © 2008 Minter-Dykhouse et al. The Rockefeller University Press.
Persistent Identifierhttp://hdl.handle.net/10722/90927
ISSN
2015 Impact Factor: 8.717
2015 SCImago Journal Rankings: 7.923
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMinterDykhouse, Ken_HK
dc.contributor.authorWard, Ien_HK
dc.contributor.authorHuen, MSYen_HK
dc.contributor.authorChen, Jen_HK
dc.contributor.authorLou, Zen_HK
dc.date.accessioned2010-09-17T10:10:28Z-
dc.date.available2010-09-17T10:10:28Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Cell Biology, 2008, v. 181 n. 5, p. 727-735en_HK
dc.identifier.issn0021-9525en_HK
dc.identifier.urihttp://hdl.handle.net/10722/90927-
dc.description.abstractThe importance of the DNA damage response (DDR) pathway in development, genomic stability, and tumor suppression is well recognized. Although 53BP1 and MDC1 have been recently identified as critical upstream mediators in the cellular response to DNA double-strand breaks, their relative hierarchy in the ataxia telangiectasia mutated (ATM) signaling cascade remains controversial. To investigate the divergent and potentially overlapping functions of MDC1 and 53BP1 in the ATM response pathway, we generated mice deficient for both genes. Unexpectedly, the loss of both MDC1 and 53BP1 neither significantly increases the severity of defects in DDR nor increases tumor incidence compared with the loss of MDC1 alone. We additionally show that MDC1 regulates 53BP1 foci formation and phosphorylation in response to DNA damage. These results suggest that MDC1 functions as an upstream regulator of 53BP1 in the DDR pathway and in tumor suppression. © 2008 Minter-Dykhouse et al. The Rockefeller University Press.en_HK
dc.languageengen_HK
dc.publisherRockefeller University Press. The Journal's web site is located at http://www.jcb.orgen_HK
dc.relation.ispartofJournal of Cell Biologyen_HK
dc.subjectSpecies Index: Ataxia Telangiectasiaen_HK
dc.subjectMusen_HK
dc.titleDistinct versus overlapping functions of MDC1 and 53BP1 in DNA damage response and tumorigenesisen_HK
dc.typeArticleen_HK
dc.identifier.emailHuen, MSY:huen.michael@hku.hken_HK
dc.identifier.authorityHuen, MSY=rp01336en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1083/jcb.200801083en_HK
dc.identifier.pmid18504301-
dc.identifier.pmcidPMC2396806-
dc.identifier.scopuseid_2-s2.0-44649164582en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-44649164582&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume181en_HK
dc.identifier.issue5en_HK
dc.identifier.spage727en_HK
dc.identifier.epage735en_HK
dc.identifier.isiWOS:000256593800003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMinterDykhouse, K=6505811795en_HK
dc.identifier.scopusauthoridWard, I=7202055968en_HK
dc.identifier.scopusauthoridHuen, MSY=23004751500en_HK
dc.identifier.scopusauthoridChen, J=35261693300en_HK
dc.identifier.scopusauthoridLou, Z=7101735844en_HK

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