FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2130818527> ?p ?o ?g. }

• W2130818527 endingPage "4444" @default.
• W2130818527 startingPage "4436" @default.
• W2130818527 abstract "Two of the hallmarks of Cockayne's syndrome (CS) are the hypersensitivity of cells to UV light and the lack of recovery of the ability to synthesize RNA following exposure of cells to UV light, in spite of the normal repair capacity at the overall genome level. The prolonged repressed RNA synthesis has been attributed to a defect in transcription-coupled repair, resulting in slow removal of DNA lesions from the transcribed strand of active genes. This model predicts that the sensitivity of CS cells to another DNA-damaging agent, i.e., the UV-mimetic agent N-acetoxy-2-acetylaminofluorene (NA-AAF), should also be associated with a lack of resumption of RNA synthesis and defective transcription-coupled repair of NA-AAF-induced DNA adducts. We tested this by measuring the rate of excision of DNA adducts in the adenosine deaminase gene of primary normal human fibroblasts and two CS (complementation group A and B) fibroblast strains. High-performance liquid chromatography analysis of DNA adducts revealed that N-(deoxyguanosin-8-yl)-2-aminofluorene (dG-C8-AF) was the main adduct induced by NA-AAF in both normal and CS cells. No differences were found between normal and CS cells with respect to induction of this lesion either at the level of the genome overall or at the gene level. Moreover, repair of dG-C8-AF in the active adenosine deaminase gene occurred at similar rates and without strand specificity in normal and CS cells, indicating that transcription-coupled repair does not contribute significantly to repair of dG-C8-AF in active genes. Yet CS cells are threefold more sensitive to NA-AAF than are normal cells and are unable to recover the ability to synthesize RNA. Our data rule out defective transcription-coupled repair as the cause of the increased sensitivity of CS cells to DNA-damaging agents and suggest that the cellular sensitivity and the prolonged repressed RNA synthesis are primarily due to a transcription defect. We hypothesize that upon treatment of cells with either UV or NA-AAF, the basal transcription factor TFIIH becomes involved in nucleotide excision repair and that the CS gene products are involved in the conversion of TFIIH back to the transcription function. In this view, the CS proteins act as repair-transcription uncoupling factors. If the uncoupling process is defective, RNA synthesis will stay repressed, causing cellular sensitivity. Since transcription is essential for transcription-coupled repair, the CS defect will affect those lesions whose repair is predominantly transcription coupled, i.e., UV-induced cyclobutane pyrimidine dimers." @default.
• W2130818527 created "2016-06-24" @default.
• W2130818527 creator A5021584591 @default.
• W2130818527 creator A5045664918 @default.
• W2130818527 creator A5052804580 @default.
• W2130818527 creator A5055142183 @default.
• W2130818527 creator A5086151589 @default.
• W2130818527 date "1996-08-01" @default.
• W2130818527 modified "2023-10-12" @default.
• W2130818527 title "The Sensitivity of Cockayne’s Syndrome Cells to DNA-Damaging Agents Is Not due to Defective Transcription-Coupled Repair of Active Genes" @default.
• W2130818527 cites W1559438128 @default.
• W2130818527 cites W1575137033 @default.
• W2130818527 cites W1889725400 @default.
• W2130818527 cites W1964315344 @default.
• W2130818527 cites W1967221425 @default.
• W2130818527 cites W1971417566 @default.
• W2130818527 cites W1979886598 @default.
• W2130818527 cites W1981089692 @default.
• W2130818527 cites W1981900473 @default.
• W2130818527 cites W1982566674 @default.
• W2130818527 cites W1983290059 @default.
• W2130818527 cites W1984353960 @default.
• W2130818527 cites W1991214623 @default.
• W2130818527 cites W2004660918 @default.
• W2130818527 cites W2005285781 @default.
• W2130818527 cites W2011382632 @default.
• W2130818527 cites W2014669590 @default.
• W2130818527 cites W2018860604 @default.
• W2130818527 cites W2019809667 @default.
• W2130818527 cites W2028559489 @default.
• W2130818527 cites W2028692871 @default.
• W2130818527 cites W2028805078 @default.
• W2130818527 cites W2030911028 @default.
• W2130818527 cites W2035699003 @default.
• W2130818527 cites W2039068784 @default.
• W2130818527 cites W2041056855 @default.
• W2130818527 cites W2049353359 @default.
• W2130818527 cites W2051883249 @default.
• W2130818527 cites W2059901912 @default.
• W2130818527 cites W2066255476 @default.
• W2130818527 cites W2069665067 @default.
• W2130818527 cites W2084079684 @default.
• W2130818527 cites W2105675578 @default.
• W2130818527 cites W2106695633 @default.
• W2130818527 cites W2109836290 @default.
• W2130818527 cites W2130669321 @default.
• W2130818527 cites W2149077186 @default.
• W2130818527 doi "https://doi.org/10.1128/mcb.16.8.4436" @default.
• W2130818527 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/231442" @default.
• W2130818527 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8754844" @default.
• W2130818527 hasPublicationYear "1996" @default.
• W2130818527 type Work @default.
• W2130818527 sameAs 2130818527 @default.
• W2130818527 citedByCount "95" @default.
• W2130818527 countsByYear W21308185272012 @default.
• W2130818527 countsByYear W21308185272013 @default.
• W2130818527 countsByYear W21308185272014 @default.
• W2130818527 countsByYear W21308185272015 @default.
• W2130818527 countsByYear W21308185272016 @default.
• W2130818527 crossrefType "journal-article" @default.
• W2130818527 hasAuthorship W2130818527A5021584591 @default.
• W2130818527 hasAuthorship W2130818527A5045664918 @default.
• W2130818527 hasAuthorship W2130818527A5052804580 @default.
• W2130818527 hasAuthorship W2130818527A5055142183 @default.
• W2130818527 hasAuthorship W2130818527A5086151589 @default.
• W2130818527 hasBestOaLocation W21308185271 @default.
• W2130818527 hasConcept C104317684 @default.
• W2130818527 hasConcept C104451858 @default.
• W2130818527 hasConcept C134935766 @default.
• W2130818527 hasConcept C138885662 @default.
• W2130818527 hasConcept C143425029 @default.
• W2130818527 hasConcept C153911025 @default.
• W2130818527 hasConcept C178169997 @default.
• W2130818527 hasConcept C179926584 @default.
• W2130818527 hasConcept C2778378917 @default.
• W2130818527 hasConcept C2779371275 @default.
• W2130818527 hasConcept C41895202 @default.
• W2130818527 hasConcept C552990157 @default.
• W2130818527 hasConcept C55493867 @default.
• W2130818527 hasConcept C86803240 @default.
• W2130818527 hasConceptScore W2130818527C104317684 @default.
• W2130818527 hasConceptScore W2130818527C104451858 @default.
• W2130818527 hasConceptScore W2130818527C134935766 @default.
• W2130818527 hasConceptScore W2130818527C138885662 @default.
• W2130818527 hasConceptScore W2130818527C143425029 @default.
• W2130818527 hasConceptScore W2130818527C153911025 @default.
• W2130818527 hasConceptScore W2130818527C178169997 @default.
• W2130818527 hasConceptScore W2130818527C179926584 @default.
• W2130818527 hasConceptScore W2130818527C2778378917 @default.
• W2130818527 hasConceptScore W2130818527C2779371275 @default.
• W2130818527 hasConceptScore W2130818527C41895202 @default.
• W2130818527 hasConceptScore W2130818527C552990157 @default.
• W2130818527 hasConceptScore W2130818527C55493867 @default.
• W2130818527 hasConceptScore W2130818527C86803240 @default.
• W2130818527 hasIssue "8" @default.
• W2130818527 hasLocation W21308185271 @default.
• W2130818527 hasLocation W21308185272 @default.
• W2130818527 hasLocation W21308185273 @default.

• next