ArticleScience (New York, N.Y.)1997
RETRACTED: Defective transcription-coupled repair of oxidative base damage in Cockayne syndrome patients from XP group G.
Article in Science (New York, N.Y.), 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 306 citations in OpenAlex.
- The UVSSA protein is part of a genome integrity homeostasis network with links to transcription-coupled DNA repair and ATM signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The capacity of oocytes for DNA repair.Cellular and molecular life sciences : CMLS · 2018Review
- BERing the burden of damage: Pathway crosstalk and posttranslational modification of base excision repair proteins regulate DNA damage management.DNA repair · 2017Review
- Potential relationship between inadequate response to DNA damage and development of myelodysplastic syndrome.International journal of molecular sciences · 2015Review
- Mfd is required for rapid recovery of transcription following UV-induced DNA damage but not oxidative DNA damage in Escherichia coli.Journal of bacteriology · 2012Article
- Somatic mutations in aging, cancer and neurodegeneration.Mechanisms of ageing and development · 2012Review
- Analysis of the genome of the sexually transmitted insect virus Helicoverpa zea nudivirus 2.Viruses · 2012Article
- The obesity-associated Fto gene is a transcriptional coactivator.Biochemical and biophysical research communications · 2010Article
- 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
- XPG: its products and biological roles.Advances in experimental medicine and biology · 2008Review
- Increased apoptosis, p53 up-regulation, and cerebellar neuronal degeneration in repair-deficient Cockayne syndrome mice.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Yeast mother cell-specific ageing, genetic (in)stability, and the somatic mutation theory of ageing.Nucleic acids research · 2007Review
- Nucleotide excision repair and cancer.Journal of molecular histology · 2006Review
- Cooperation of the Cockayne syndrome group B protein and poly(ADP-ribose) polymerase 1 in the response to oxidative stress.Molecular and cellular biology · 2005Article
- Mitochondrial inhibition of uracil-DNA glycosylase is not mutagenic.Molecular cancer · 2004Article
- Different effects of CSA and CSB deficiency on sensitivity to oxidative DNA damage.Molecular and cellular biology · 2004Article
- Identification of the XPG region that causes the onset of Cockayne syndrome by using Xpg mutant mice generated by the cDNA-mediated knock-in method.Molecular and cellular biology · 2004Article
- Cockayne syndrome group B cellular and biochemical functions.American journal of human genetics · 2003Review
- Methylated DNA-binding domain 1 and methylpurine-DNA glycosylase link transcriptional repression and DNA repair in chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Effects of genomic context and chromatin structure on transcription-coupled and global genomic repair in mammalian cells.Nucleic acids research · 2003Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2005-06-17Investigation by Company/Institution · Investigation by Journal/Publisher · Investigation by ORI · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Unreliable Results and/or Conclusions · · NIH Finding of misconduct for Steven A Leadon, 2/9/2006; Notice paywalled as of 4.3.2022;
- Commented on by
- RetractedRetraction.2005
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
In normal human cells, damage due to ultraviolet light is preferentially removed from active genes by nucleotide excision repair (NER) in a transcription-coupled repair (TCR) process that requires the gene products defective in Cockayne syndrome (CS). Oxidative damage, including thymine glycols, is shown to be removed by TCR in cells from normal individuals and from xeroderma pigmentosum (XP)-A, XP-F, and XP-G patients who have NER defects but not from XP-G patients who have severe CS. Thus, TCR of oxidative damage requires an XPG function distinct from its NER endonuclease activity. These results raise the possibility that defective TCR of oxidative damage contributes to the developmental defects associated with CS.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.