A single 8,5′-cyclo-2′-deoxyadenosine lesion in a TATA box prevents binding of the TATA binding protein and strongly reduces transcription in vivo
- 29 August 2002
- journal article
- research article
- Published by Elsevier in DNA Repair
- Vol. 1 (11), 967-975
- https://doi.org/10.1016/s1568-7864(02)00148-9
Abstract
No abstract availableKeywords
This publication has 38 references indexed in Scilit:
- The contribution of endogenous sources of DNA damage to the multiple mutations in cancerMutation Research, 2001
- The Oxidative DNA Lesion 8,5′-(S)-Cyclo-2′-deoxyadenosine Is Repaired by the Nucleotide Excision Repair Pathway and Blocks Gene Expression in Mammalian CellsJournal of Biological Chemistry, 2000
- Removal of oxygen free-radical-induced 5′,8-purine cyclodeoxynucleosides from DNA by the nucleotide excision-repair pathway in human cellsProceedings of the National Academy of Sciences, 2000
- Quality Control by DNA RepairScience, 1999
- Reactions of oxyl radicals with DNAFree Radical Biology & Medicine, 1995
- DNA excision-repair defect of xeroderma pigmentosum prevents removal of a class of oxygen free radical-induced base lesions.Proceedings of the National Academy of Sciences, 1993
- Instability and decay of the primary structure of DNANature, 1993
- Oxidative damage to DNA in mammalian chromatinMutation Research/DNAging, 1992
- A Childhood Neurodegeneration Due to Defective DNA Repair: A Novel Concept of Disease Based on Studies of Xeroderma PigmentosumJournal of Child Neurology, 1989
- Xeroderma pigmentosum neurological abnormalities correlate with colony-forming ability after ultraviolet radiation.Proceedings of the National Academy of Sciences, 1978