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DC Field | Value | Language |
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dc.citation.endPage | 444 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 438 | - |
dc.citation.title | DNA REPAIR | - |
dc.citation.volume | 10 | - |
dc.contributor.author | Krijger, Peter H. L. | - |
dc.contributor.author | Lee, Kyoo-Young | - |
dc.contributor.author | Wit, Niek | - |
dc.contributor.author | van den Berk, Paul C. M. | - |
dc.contributor.author | Wu, Xiaoli | - |
dc.contributor.author | Roest, Henk P. | - |
dc.contributor.author | Maas, Alex | - |
dc.contributor.author | Ding, Hao | - |
dc.contributor.author | Hoeijmakers, Jan H. J. | - |
dc.contributor.author | Myung, Kyungjae | - |
dc.contributor.author | Jacobs, Heinz | - |
dc.date.accessioned | 2023-12-22T06:11:57Z | - |
dc.date.available | 2023-12-22T06:11:57Z | - |
dc.date.created | 2020-01-31 | - |
dc.date.issued | 2011-04 | - |
dc.description.abstract | DNA damage tolerance is regulated at least in part at the level of proliferating cell nuclear antigen (PCNA) ubiquitination. Monoubiquitination (PCNA-Ub) at lysine residue 164 (K164) stimulates error-prone translesion synthesis (US), Rad5-dependent polyubiquitination (PCNA-Ub(n)) stimulates error-free template switching (TS). To generate high affinity antibodies by somatic hypermutation (SHM), B cells profit from error-prone TLS polymerases. Consistent with the role of PCNA-Ub in stimulating TLS, hypermutated B cells of PCNA(K164R) mutant mice display a defect in generating selective point mutations. Two Rad5 orthologs, HLTF and SHPRH have been identified as alternative E3 ligases generating PCNA-Ub(n) in mammals. As PCNA-Ub and PCNA-Ub(n) both make use of K164, error-free PCNA-Ub(n)-dependent TS may suppress error-prone PCNA-Ub-dependent TLS. To determine a regulatory role of Shprh and Hltf in SHM, we generated Shprh/Hltf double mutant mice. Interestingly, while the formation of PCNA-Ub and PCNA-Ub(n) is prohibited in PCNA(K164R) MEFs, the formation of PCNA-Ub(n) is not abolished in Shprh/Hltf mutant MEFs. In line with these observations Shprh/Hltf double mutant B cells were not hypersensitive to DNA damage. Furthermore, SHM was normal in Shprh/Hltf mutant B cells. These data suggest the existence of an alternative E3 ligase in the generation of PCNA-Ub(n). | - |
dc.identifier.bibliographicCitation | DNA REPAIR, v.10, no.4, pp.438 - 444 | - |
dc.identifier.doi | 10.1016/j.dnarep.2010.12.008 | - |
dc.identifier.issn | 1568-7864 | - |
dc.identifier.scopusid | 2-s2.0-79952708049 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/31045 | - |
dc.identifier.url | https://www.sciencedirect.com/science/article/pii/S1568786410004179?via%3Dihub | - |
dc.identifier.wosid | 000289596400010 | - |
dc.language | 영어 | - |
dc.publisher | ELSEVIER SCIENCE BV | - |
dc.title | HLTF and SHPRH are not essential for PCNA polyubiquitination, survival and somatic hypermutation: Existence of an alternative E3 ligase | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Genetics & Heredity; Toxicology | - |
dc.relation.journalResearchArea | Genetics & Heredity; Toxicology | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | PCNA | - |
dc.subject.keywordAuthor | RAD5 | - |
dc.subject.keywordAuthor | HLTF | - |
dc.subject.keywordAuthor | SHPRH | - |
dc.subject.keywordAuthor | Somatic hypermutation | - |
dc.subject.keywordAuthor | Translesion synthesis | - |
dc.subject.keywordPlus | CELL NUCLEAR ANTIGEN | - |
dc.subject.keywordPlus | DNA-POLYMERASE-ETA | - |
dc.subject.keywordPlus | IMMUNOGLOBULIN GENE HYPERMUTATION | - |
dc.subject.keywordPlus | POSTREPLICATION REPAIR PATHWAY | - |
dc.subject.keywordPlus | CLASS-SWITCH RECOMBINATION | - |
dc.subject.keywordPlus | SACCHAROMYCES-CEREVISIAE | - |
dc.subject.keywordPlus | TRANSLESION SYNTHESIS | - |
dc.subject.keywordPlus | UBIQUITIN LIGASE | - |
dc.subject.keywordPlus | GENOMIC INSTABILITY | - |
dc.subject.keywordPlus | DAMAGE | - |
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