ArticleMolecular and cellular biology2002
Yeast RAD26, a homolog of the human CSB gene, functions independently of nucleotide excision repair and base excision repair in promoting transcription through damaged bases.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- The ARK2N-CK2 complex initiates transcription-coupled repair through enhancing the interaction of CSB with lesion-stalled RNAPII.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- DNA Repair in Haploid Context.International journal of molecular sciences · 2021Review
- Epigenetics Identifier screens reveal regulators of chromatin acylation and limited specificity of acylation antibodies.Scientific reports · 2021Article
- Nucleotide excision repair of abasic DNA lesions.Nucleic acids research · 2019Article
- Ribosome biogenesis factor Ltv1 chaperones the assembly of the small subunit head.The Journal of cell biology · 2018Article
- Translational Reprogramming Provides a Blueprint for Cellular Adaptation.Cell chemical biology · 2018Article
- Genome-wide maps of alkylation damage, repair, and mutagenesis in yeast reveal mechanisms of mutational heterogeneity.Genome research · 2017Article
- Nucleotide excision repair in Trypanosoma brucei: specialization of transcription-coupled repair due to multigenic transcription.Molecular microbiology · 2014Article
- Yeast RAD2, a homolog of human XPG, plays a key role in the regulation of the cell cycle and actin dynamics.Biology open · 2014Article
- Regulation of active genome integrity and expression by Rad26p.Nucleus (Austin, Tex.) · 2014Review
- Chromatin modifications and DNA repair: beyond double-strand breaks.Frontiers in genetics · 2014Review
- Review
- Functional analysis of Rad14p, a DNA damage recognition factor in nucleotide excision repair, in regulation of transcription in vivo.The Journal of biological chemistry · 2013Article
- Preferential repair of DNA double-strand break at the active gene in vivo.The Journal of biological chemistry · 2012Article
- Rad26p, a transcription-coupled repair factor, promotes the eviction and prevents the reassociation of histone H2A-H2B dimer during transcriptional elongation in vivo.Biochemistry · 2012Article
- Rad26p regulates the occupancy of histone H2A-H2B dimer at the active genes in vivo.Nucleic acids research · 2012Article
- The mRNA cap-binding complex stimulates the formation of pre-initiation complex at the promoter via its interaction with Mot1p in vivo.Nucleic acids research · 2011Article
- Rad26p, a transcription-coupled repair factor, is recruited to the site of DNA lesion in an elongating RNA polymerase II-dependent manner in vivo.Nucleic acids research · 2010Article
- ATP-dependent chromatin remodeling factors and DNA damage repair.Mutation research · 2007Review
- Initiation of DNA repair mediated by a stalled RNA polymerase IIO.The EMBO journal · 2006Article
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Authors and funding
4 authors.
Funding
Abstract
RAD26 in the yeast Saccharomyces cerevisiae is the counterpart of the human Cockayne syndrome group B (CSB) gene. Both RAD26 and CSB act in the preferential repair of UV lesions on the transcribed strand, and in this process, they function together with the components of nucleotide excision repair (NER). Here, we examine the role of RAD26 in the repair of DNA lesions induced upon treatment with the alkylating agent methyl methanesulfonate (MMS). MMS-induced DNA lesions include base damages such as 3-methyl adenine and 7-methyl guanine, and these lesions are removed in yeast by the alternate competing pathways of base excision repair (BER), which is initiated by the action of MAG1-encoded N-methyl purine DNA glycosylase, and NER. Interestingly, a synergistic increase in MMS sensitivity was observed in the rad26 Delta strain upon inactivation of NER or BER, indicating that RAD26 promotes the survival of MMS-treated cells by a mechanism that acts independently of either of these repair pathways. The galactose-inducible transcription of the GAL2, GAL7, and GAL10 genes is reduced in MMS-treated rad26 Delta cells and also in mag1 Delta rad14 Delta cells, whereas a very severe reduction in transcription occurs in MMS-treated mag1 Delta rad14 Delta rad26 Delta cells. From these observations, we infer that RAD26 plays a role in promoting transcription by RNA polymerase II through damaged bases. The implications of these observations are discussed in this paper.
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