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- Publisher Website: 10.1083/jcb.200801083
- Scopus: eid_2-s2.0-44649164582
- PMID: 18504301
- WOS: WOS:000256593800003
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Article: Distinct versus overlapping functions of MDC1 and 53BP1 in DNA damage response and tumorigenesis
Title | Distinct versus overlapping functions of MDC1 and 53BP1 in DNA damage response and tumorigenesis |
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Authors | |
Keywords | Species Index: Ataxia Telangiectasia Mus |
Issue Date | 2008 |
Publisher | Rockefeller 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? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/90927 |
ISSN | 2021 Impact Factor: 8.077 2020 SCImago Journal Rankings: 5.414 |
PubMed Central ID | |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | MinterDykhouse, K | en_HK |
dc.contributor.author | Ward, I | en_HK |
dc.contributor.author | Huen, MSY | en_HK |
dc.contributor.author | Chen, J | en_HK |
dc.contributor.author | Lou, Z | en_HK |
dc.date.accessioned | 2010-09-17T10:10:28Z | - |
dc.date.available | 2010-09-17T10:10:28Z | - |
dc.date.issued | 2008 | en_HK |
dc.identifier.citation | Journal Of Cell Biology, 2008, v. 181 n. 5, p. 727-735 | en_HK |
dc.identifier.issn | 0021-9525 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/90927 | - |
dc.description.abstract | The 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.language | eng | en_HK |
dc.publisher | Rockefeller University Press. The Journal's web site is located at http://www.jcb.org | en_HK |
dc.relation.ispartof | Journal of Cell Biology | en_HK |
dc.subject | Species Index: Ataxia Telangiectasia | en_HK |
dc.subject | Mus | en_HK |
dc.title | Distinct versus overlapping functions of MDC1 and 53BP1 in DNA damage response and tumorigenesis | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Huen, MSY:huen.michael@hku.hk | en_HK |
dc.identifier.authority | Huen, MSY=rp01336 | en_HK |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1083/jcb.200801083 | en_HK |
dc.identifier.pmid | 18504301 | - |
dc.identifier.pmcid | PMC2396806 | - |
dc.identifier.scopus | eid_2-s2.0-44649164582 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-44649164582&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 181 | en_HK |
dc.identifier.issue | 5 | en_HK |
dc.identifier.spage | 727 | en_HK |
dc.identifier.epage | 735 | en_HK |
dc.identifier.isi | WOS:000256593800003 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | MinterDykhouse, K=6505811795 | en_HK |
dc.identifier.scopusauthorid | Ward, I=7202055968 | en_HK |
dc.identifier.scopusauthorid | Huen, MSY=23004751500 | en_HK |
dc.identifier.scopusauthorid | Chen, J=35261693300 | en_HK |
dc.identifier.scopusauthorid | Lou, Z=7101735844 | en_HK |
dc.identifier.issnl | 0021-9525 | - |