pubmed-article:9150142 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9150142 | lifeskim:mentions | umls-concept:C0007114 | lld:lifeskim |
pubmed-article:9150142 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:9150142 | lifeskim:mentions | umls-concept:C0009207 | lld:lifeskim |
pubmed-article:9150142 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
pubmed-article:9150142 | lifeskim:mentions | umls-concept:C0220898 | lld:lifeskim |
pubmed-article:9150142 | lifeskim:mentions | umls-concept:C1158557 | lld:lifeskim |
pubmed-article:9150142 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:9150142 | pubmed:dateCreated | 1997-6-6 | lld:pubmed |
pubmed-article:9150142 | pubmed:abstractText | A mouse model for the nucleotide excision repair disorder Cockayne syndrome (CS) was generated by mimicking a truncation in the CSB(ERCC6) gene of a CS-B patient. CSB-deficient mice exhibit all of the CS repair characteristics: ultraviolet (UV) sensitivity, inactivation of transcription-coupled repair, unaffected global genome repair, and inability to resume RNA synthesis after UV exposure. Other CS features thought to involve the functioning of basal transcription/repair factor TFIIH, such as growth failure and neurologic dysfunction, are present in mild form. In contrast to the human syndrome, CSB-deficient mice show increased susceptibility to skin cancer. Our results demonstrate that transcription-coupled repair of UV-induced cyclobutane pyrimidine dimers contributes to the prevention of carcinogenesis in mice. Further, they suggest that the lack of cancer predisposition in CS patients is attributable to a global genome repair process that in humans is more effective than in rodents. | lld:pubmed |
pubmed-article:9150142 | pubmed:language | eng | lld:pubmed |
pubmed-article:9150142 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9150142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9150142 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9150142 | pubmed:month | May | lld:pubmed |
pubmed-article:9150142 | pubmed:issn | 0092-8674 | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:BootsmaDD | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:de WitJJ | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:HoeijmakersJ... | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:van SteegHH | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:BeemsR BRB | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:WeedaGG | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:MorreauHH | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:van der... | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:de GruijlF... | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:van KreijlC... | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:AONOKK | lld:pubmed |
pubmed-article:9150142 | pubmed:author | pubmed-author:van GoolA JAJ | lld:pubmed |
pubmed-article:9150142 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9150142 | pubmed:day | 2 | lld:pubmed |
pubmed-article:9150142 | pubmed:volume | 89 | lld:pubmed |
pubmed-article:9150142 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9150142 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9150142 | pubmed:pagination | 425-35 | lld:pubmed |
pubmed-article:9150142 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:9150142 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9150142 | pubmed:articleTitle | Defective transcription-coupled repair in Cockayne syndrome B mice is associated with skin cancer predisposition. | lld:pubmed |
pubmed-article:9150142 | pubmed:affiliation | Medical Genetics Center, Department of Cell Biology and Genetics, Erasmus University Rotterdam, The Netherlands. | lld:pubmed |
pubmed-article:9150142 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9150142 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:319955 | entrezgene:pubmed | pubmed-article:9150142 | lld:entrezgene |
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