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- W2019414523 endingPage "252" @default.
- W2019414523 startingPage "243" @default.
- W2019414523 abstract "Bulky DNA adducts induced by agents like ultraviolet light, cisplatin and oxidative metabolism pose a block to elongation by RNA polymerase II (RNAPII). The arrested RNAPII can initiate the repair of transcription-blocking DNA lesions by transcription-coupled nucleotide excision repair (TC-NER) to permit efficient recovery of mRNA synthesis while widespread sustained transcription blocks lead to apoptosis. Therefore, RNAPII serves as a processive DNA damage sensor that identifies transcription-blocking DNA lesions. Cockayne syndrome (CS) is an autosomal recessive disorder characterized by a complex phenotype that includes clinical photosensitivity, progressive neurological degeneration and premature-aging. CS is associated with defects in TC-NER and the recovery of mRNA synthesis, making CS cells exquisitely sensitive to a variety of DNA damaging agents. These defects in the coupling of repair and transcription appear to underlie some of the complex clinical features of CS. Recent insight into the consequences of blocked transcription and their relationship to CS will be discussed." @default.
- W2019414523 created "2016-06-24" @default.
- W2019414523 creator A5030941843 @default.
- W2019414523 creator A5049615740 @default.
- W2019414523 date "2013-05-01" @default.
- W2019414523 modified "2023-10-16" @default.
- W2019414523 title "Arresting transcription and sentencing the cell: The consequences of blocked transcription" @default.
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