Article: RAD18-BRCTx interaction is required for efficient repair of UV-induced DNA damage

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TitleRAD18-BRCTx interaction is required for efficient repair of UV-induced DNA damage
AuthorsLiu, T2
Chen, H2
Kim, H4
Huen, MSY1
Chen, J3
Huang, J2
KeywordsBRCT domain
DNA damage
DNA repair
RAD18
Issue Date2012
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/dnarepair
CitationDna Repair, 2012, v. 11 n. 2, p. 131-138 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.dnarep.2011.10.012
AbstractBRCA1 carboxyl-terminal (BRCT) motifs are present in a number of proteins involved in DNA repair and/or DNA damage signaling pathways. The BRCT domain-containing protein BRCTx has been shown to interact physically with RAD18, an E3 ligase involved in postreplication repair and homologous recombination repair. However, the physiological relevance of the interaction between RAD18 and BRCTx is largely unknown. In this study, we showed that RAD18 interacts with BRCTx in a phosphorylation-dependent manner and that this interaction, mediated via highly conserved serine residues on the RAD18 C terminus, is required for BRCTx accumulation at DNA damage sites. Furthermore, we uncovered critical roles of the RAD18-BRCTx module in UV-induced DNA damage repair but not PCNA mono-ubiquitination or homologous recombination. Thus, our results suggest that RAD18 has an additional function in the surveillance of the UV-induced DNA damage response signal. © 2011 Elsevier B.V..
ISSN1568-7864
2011 Impact Factor: 4.135
2011 SCImago Journal Rankings: 0.773
DOIhttp://dx.doi.org/10.1016/j.dnarep.2011.10.012
ISI Accession Number IDWOS:000301618900005
Funding AgencyGrant Number
National Natural Science Foundation of China31071243
Natural Science Foundation of Zhejiang ProvinceR2110569
China's Fundamental Research Funds for the Central Universities
Department of DefenseW81XWH-05-1-0470
Funding Information:

We would like to thank Dr. M. Yamaizumi for providing RAD18-/- MEFs and all our colleagues in the Huang laboratory for insightful discussions and technical assistance. This work was supported in part by grants from the National Natural Science Foundation of China (grant 31071243), the Natural Science Foundation of Zhejiang Province (grant R2110569) and the China's Fundamental Research Funds for the Central Universities. J.C. is a recipient of an Era of Hope Scholar award from the Department of Defense (W81XWH-05-1-0470) and a member of MD Anderson Cancer Center (CA016672).

ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorLiu, T
dc.contributor.authorChen, H
dc.contributor.authorKim, H
dc.contributor.authorHuen, MSY
dc.contributor.authorChen, J
dc.contributor.authorHuang, J
dc.date.accessioned2012-02-03T06:11:41Z
dc.date.available2012-02-03T06:11:41Z
dc.date.issued2012
dc.description.abstractBRCA1 carboxyl-terminal (BRCT) motifs are present in a number of proteins involved in DNA repair and/or DNA damage signaling pathways. The BRCT domain-containing protein BRCTx has been shown to interact physically with RAD18, an E3 ligase involved in postreplication repair and homologous recombination repair. However, the physiological relevance of the interaction between RAD18 and BRCTx is largely unknown. In this study, we showed that RAD18 interacts with BRCTx in a phosphorylation-dependent manner and that this interaction, mediated via highly conserved serine residues on the RAD18 C terminus, is required for BRCTx accumulation at DNA damage sites. Furthermore, we uncovered critical roles of the RAD18-BRCTx module in UV-induced DNA damage repair but not PCNA mono-ubiquitination or homologous recombination. Thus, our results suggest that RAD18 has an additional function in the surveillance of the UV-induced DNA damage response signal. © 2011 Elsevier B.V..
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationDna Repair, 2012, v. 11 n. 2, p. 131-138 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.dnarep.2011.10.012
dc.identifier.citeulike10008825
dc.identifier.doihttp://dx.doi.org/10.1016/j.dnarep.2011.10.012
dc.identifier.epage138
dc.identifier.hkuros198267
dc.identifier.isiWOS:000301618900005
Funding AgencyGrant Number
National Natural Science Foundation of China31071243
Natural Science Foundation of Zhejiang ProvinceR2110569
China's Fundamental Research Funds for the Central Universities
Department of DefenseW81XWH-05-1-0470
Funding Information:

We would like to thank Dr. M. Yamaizumi for providing RAD18-/- MEFs and all our colleagues in the Huang laboratory for insightful discussions and technical assistance. This work was supported in part by grants from the National Natural Science Foundation of China (grant 31071243), the Natural Science Foundation of Zhejiang Province (grant R2110569) and the China's Fundamental Research Funds for the Central Universities. J.C. is a recipient of an Era of Hope Scholar award from the Department of Defense (W81XWH-05-1-0470) and a member of MD Anderson Cancer Center (CA016672).

dc.identifier.issn1568-7864
2011 Impact Factor: 4.135
2011 SCImago Journal Rankings: 0.773
dc.identifier.issue2
dc.identifier.pmid22036607
dc.identifier.scopuseid_2-s2.0-84855851489
dc.identifier.spage131
dc.identifier.urihttp://hdl.handle.net/10722/144510
dc.identifier.volume11
dc.languageeng
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/dnarepair
dc.publisher.placeNetherlands
dc.relation.ispartofDNA Repair
dc.relation.referencesReferences in Scopus
dc.subjectBRCT domain
dc.subjectDNA damage
dc.subjectDNA repair
dc.subjectRAD18
dc.titleRAD18-BRCTx interaction is required for efficient repair of UV-induced DNA damage
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Zhejiang University
  3. University of Texas M. D. Anderson Cancer Center
  4. Sungkyunkwan University