ArticleNucleic acids research2000
Molecular characterization of an acidic region deletion mutant of Cockayne syndrome group B protein.
Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Role of Cockayne Syndrome Group B Protein in Replication Stress: Implications for Cancer Therapy.International journal of molecular sciences · 2022Review
- Current and emerging roles of Cockayne syndrome group B (CSB) protein.Nucleic acids research · 2021Review
- Cockayne Syndrome: The many challenges and approaches to understand a multifaceted disease.Genetics and molecular biology · 2020Article
- Tethering of the conserved piggyBac transposase fusion protein CSB-PGBD3 to chromosomal AP-1 proteins regulates expression of nearby genes in humans.PLoS genetics · 2012Article
- UV-induced association of the CSB remodeling protein with chromatin requires ATP-dependent relief of N-terminal autorepression.Molecular cell · 2010Article
- Nucleic acid binding activity of human Cockayne syndrome B protein and identification of Ca(2+) as a novel metal cofactor.Journal of molecular biology · 2009Article
- An abundant evolutionarily conserved CSB-PiggyBac fusion protein expressed in Cockayne syndrome.PLoS genetics · 2008Article
- Cockayne syndrome B protein stimulates apurinic endonuclease 1 activity and protects against agents that introduce base excision repair intermediates.Nucleic acids research · 2007Article
- Cockayne syndrome group B cellular and biochemical functions.American journal of human genetics · 2003Review
- Functional consequences of mutations in the conserved SF2 motifs and post-translational phosphorylation of the CSB protein.Nucleic acids research · 2003Article
- Global genome repair of 8-oxoG in hamster cells requires a functional CSB gene product.Oncogene · 2002Article
- What role (if any) does the highly conserved CSB-PGBD3 fusion protein play in Cockayne syndrome?Mechanisms of ageing and developmentReview
- The role of Cockayne Syndrome group B (CSB) protein in base excision repair and aging.Mechanisms of ageing and developmentReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cockayne syndrome (CS) is a human genetic disorder characterized by post-natal growth failure, neurological abnormalities and premature aging. CS cells exhibit high sensitivity to UV light, delayed RNA synthesis recovery after UV irradiation and defective transcription-coupled repair (TCR). Two genetic complementation groups of CS have been identified, designated CS-A and CS-B. The CSB gene encodes a helicase domain and a highly acidic region N-terminal to the helicase domain. This study describes the genetic characterization of a CSB mutant allele encoding a full deletion of the acidic region. We have tested its ability to complement the sensitivity of UV61, the hamster homolog of human CS-B cells, to UV and the genotoxic agent N-acetoxy-2-acetylaminofluorene (NA-AAF). Deleting 39 consecutive amino acids, of which approximately 60% are negatively charged, did not impact on the ability of the protein to complement the sensitive phenotype of UV61 cells to either UV or NA-AAF. Our data indicate that the highly acidic region of CSB is not essential for the TCR and general genome repair pathways of UV- and NA-AAF-induced DNA lesions.
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