ArticleMolecular and cellular biology2005
Transcription-associated breaks in xeroderma pigmentosum group D cells from patients with combined features of xeroderma pigmentosum and Cockayne syndrome.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Persistent TFIIH binding to non-excised DNA damage causes cell and developmental failure.Nature communications · 2024Article
- aniFOUND: analysing the associated proteome and genomic landscape of the repaired nascent non-replicative chromatin.Nucleic acids research · 2021Article
- The DNA damage response network in the treatment of head and neck squamous cell carcinoma.ESMO open · 2021Article
- Envisioning how the prototypic molecular machine TFIIH functions in transcription initiation and DNA repair.DNA repair · 2020Review
- Evolving insights: how DNA repair pathways impact cancer evolution.Cancer biology & medicine · 2020Review
- Defective transcription of ATF3 responsive genes, a marker for Cockayne Syndrome.Scientific reports · 2020Article
- Article
- The Structures of Eukaryotic Transcription Pre-initiation Complexes and Their Functional Implications.Sub-cellular biochemistry · 2019Review
- Constructive rescue of TFIIH instability by an alternative isoform of XPD derived from a mutated XPD allele in mild but not severe XP-D/CS.Journal of human genetics · 2015Article
- A Drosophila XPD model links cell cycle coordination with neuro-development and suggests links to cancer.Disease models & mechanisms · 2015Article
- The rem mutations in the ATP-binding groove of the Rad3/XPD helicase lead to Xeroderma pigmentosum-Cockayne syndrome-like phenotypes.PLoS genetics · 2014Article
- Sirt1 suppresses RNA synthesis after UV irradiation in combined xeroderma pigmentosum group D/Cockayne syndrome (XP-D/CS) cells.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Generation of DNA single-strand displacement by compromised nucleotide excision repair.The EMBO journal · 2012Article
- Transcription inhibition by DRB potentiates recombinational repair of UV lesions in mammalian cells.PloS one · 2011Article
- UV-induced histone H2AX phosphorylation and DNA damage related proteins accumulate and persist in nucleotide excision repair-deficient XP-B cells.DNA repair · 2011Article
- Coordination of dual incision and repair synthesis in human nucleotide excision repair.The EMBO journal · 2009Article
- Review
- Structure of the DNA repair helicase XPD.Cell · 2008Article
- Article
- Hot topics in DNA repair: the molecular basis for different disease states caused by mutations in TFIIH and XPG.DNA repair · 2008Review
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defects in the XPD gene can result in several clinical phenotypes, including xeroderma pigmentosum (XP), trichothiodystrophy, and, less frequently, the combined phenotype of XP and Cockayne syndrome (XP-D/CS). We previously showed that in cells from two XP-D/CS patients, breaks were introduced into cellular DNA on exposure to UV damage, but these breaks were not at the sites of the damage. In the present work, we show that three further XP-D/CS patients show the same peculiar breakage phenomenon. We show that these breaks can be visualized inside the cells by immunofluorescence using antibodies to either gamma-H2AX or poly-ADP-ribose and that they can be generated by the introduction of plasmids harboring methylation or oxidative damage as well as by UV photoproducts. Inhibition of RNA polymerase II transcription by four different inhibitors dramatically reduced the number of UV-induced breaks. Furthermore, the breaks were dependent on the nucleotide excision repair (NER) machinery. These data are consistent with our hypothesis that the NER machinery introduces the breaks at sites of transcription initiation. During transcription in UV-irradiated XP-D/CS cells, phosphorylation of the carboxy-terminal domain of RNA polymerase II occurred normally, but the elongating form of the polymerase remained blocked at lesions and was eventually degraded.
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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.