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- DNA damage4
- nucleotide excision repair4
- transcription-coupled repair3
- chemotherapy2
- excision repair sequencing (XR-seq)2
- genomics2
- bioinformatics1
- chemoresistance1
- chronotherapy1
- circadian clock1
- cisplatin1
- colorectal cancer1
- cytotoxicity1
- DNA adduct1
- DNA sequencing1
- DNA transcription1
- drug resistance1
- Escherichia coli (E. coli)1
- gene transcription1
- kinetics1
- Mfd1
- RNA polymerase II1
- UvrD1
- XR-seq1
DNA and Chromosomes
5 Results
- DNA and ChromosomesOpen Access
Genome-wide single-nucleotide resolution of oxaliplatin–DNA adduct repair in drug-sensitive and -resistant colorectal cancer cell lines
Journal of Biological ChemistryVol. 295Issue 22p7584–7594Published online: April 16, 2020- Courtney M. Vaughn
- Christopher P. Selby
- Yanyan Yang
- David S. Hsu
- Aziz Sancar
Cited in Scopus: 11Platinum-based chemotherapies, including oxaliplatin, are a mainstay in the management of solid tumors and induce cell death by forming intrastrand dinucleotide DNA adducts. Despite their common use, they are highly toxic, and approximately half of cancer patients have tumors that are either intrinsically resistant or develop resistance. Previous studies suggest that this resistance is mediated by variations in DNA repair levels or net drug influx. Here, we aimed to better define the roles of nucleotide excision repair and DNA damage in platinum chemotherapy resistance by profiling DNA damage and repair efficiency in seven oxaliplatin-sensitive and three oxaliplatin-resistant colorectal cancer cell lines. - DNA and ChromosomesOpen Access
Long-term, genome-wide kinetic analysis of the effect of the circadian clock and transcription on the repair of cisplatin-DNA adducts in the mouse liver
Journal of Biological ChemistryVol. 294Issue 32p11960–11968Published online: June 19, 2019- Yanyan Yang
- Zhenxing Liu
- Christopher P. Selby
- Aziz Sancar
Cited in Scopus: 15Cisplatin is the most commonly used chemotherapeutic drug for managing solid tumors. However, toxicity and the innate or acquired resistance of cancer cells to the drug limit its usefulness. Cisplatin kills cells by forming cisplatin-DNA adducts, most commonly the Pt-d(GpG) diadduct. We recently showed that, in mice, repair of this adduct 2 h following injection is controlled by two circadian programs. 1) The circadian clock controls transcription of 2000 genes in liver and, via transcription-directed repair, controls repair of the transcribed strand (TS) of these genes in a rhythmic fashion unique to each gene’s phase of transcription. - DNA and ChromosomesOpen Access
Single-nucleotide resolution analysis of nucleotide excision repair of ribosomal DNA in humans and mice
Journal of Biological ChemistryVol. 294Issue 1p210–217Published online: November 9, 2018- Yanyan Yang
- Jinchuan Hu
- Christopher P. Selby
- Wentao Li
- Askar Yimit
- Yuchao Jiang
- and others
Cited in Scopus: 12The unique nucleolar environment, the repetitive nature of ribosomal DNA (rDNA), and especially the possible involvement of RNA polymerase I (RNAPI) in transcription-coupled repair (TCR) have made the study of repair of rDNA both interesting and challenging. TCR, the transcription-dependent, preferential excision repair of the template strand compared with the nontranscribed (coding) strand has been clearly demonstrated in genes transcribed by RNAPII. Whether TCR occurs in rDNA is unresolved. In the present work, we have applied analytical methods to map repair events in rDNA using data generated by the newly developed XR-seq procedure, which measures excision repair genome-wide with single-nucleotide resolution. - DNA and ChromosomesOpen Access
RNA polymerase II is released from the DNA template during transcription-coupled repair in mammalian cells
Journal of Biological ChemistryVol. 293Issue 7p2476–2486Published online: December 27, 2017- Yi-Ying Chiou
- Jinchuan Hu
- Aziz Sancar
- Christopher P. Selby
Cited in Scopus: 33In mammalian cells, bulky DNA adducts located in the template but not the coding strand of genes block elongation by RNA polymerase II (RNAPII). The blocked RNAPII targets these transcription-blocking adducts to undergo more rapid excision repair than adducts located elsewhere in the genome. In excision repair, coupled incisions are made in the damaged DNA strand on both sides of the adduct. The fate of RNAPII in the course of this transcription-coupled repair (TCR) pathway is unclear. To address the fate of RNAPII, we used methods that control transcription to initiate a discrete “wave” of elongation complexes. - Accelerated CommunicationsOpen Access
Mfd translocase is necessary and sufficient for transcription-coupled repair in Escherichia coli
Journal of Biological ChemistryVol. 292Issue 45p18386–18391Published online: October 6, 2017- Ogun Adebali
- Aziz Sancar
- Christopher P. Selby
Cited in Scopus: 29Nucleotide excision repair in Escherichia coli is stimulated by transcription, specifically in the transcribed strand. Previously, it was shown that this transcription-coupled repair (TCR) is mediated by the Mfd translocase. Recently, it was proposed that in fact the majority of TCR in E. coli is catalyzed by a second pathway (“backtracking-mediated TCR”) that is dependent on the UvrD helicase and the guanosine pentaphosphate (ppGpp) alarmone/stringent response regulator. Recently, we reported that as measured by the excision repair–sequencing (XR-seq), UvrD plays no role in TCR genome-wide.