Results 311 to 320 of about 98,783 (332)
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Nucleotide excision repair in yeast
Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 2000In nucleotide excision repair (NER) in eukaryotes, DNA is incised on both sides of the lesion, resulting in the removal of a fragment approximately 25-30 nucleotides long. This is followed by repair synthesis and ligation. The proteins encoded by the various yeast NER genes have been purified, and the incision reaction reconstituted in vitro.
S, Prakash, L, Prakash
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2017
Lung cancer is a particularly devastating disease, accounting for the most deaths among all cancer types in the United States. Despite a reduction in the country’s smoking rates, cigarette smoking remains the number one risk factor for lung cancer. Additionally arsenic exposure, which occurs primarily through contaminated drinking water in the U.S., is
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Lung cancer is a particularly devastating disease, accounting for the most deaths among all cancer types in the United States. Despite a reduction in the country’s smoking rates, cigarette smoking remains the number one risk factor for lung cancer. Additionally arsenic exposure, which occurs primarily through contaminated drinking water in the U.S., is
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Chromatin rearrangements during nucleotide excision repair
Biochimie, 1999The removal of DNA damage from the eukaryotic genome requires DNA repair enzymes to operate within the complex environment of chromatin. We review the evidence for chromatin rearrangements during nucleotide excision repair and discuss the extent and possible molecular mechanisms of these rearrangements, focusing on events at the nucleosome level of ...
J G, Moggs, G, Almouzni
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Genomic heterogeneity of nucleotide excision repair
Gene, 2000Nucleotide excision repair (NER) is one of the major cellular pathways that removes bulky DNA adducts and helix-distorting lesions. The biological consequences of defective NER in humans include UV-light-induced skin carcinogenesis and extensive neurodegeneration.
A S, Balajee, V A, Bohr
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Disorders of nucleotide excision repair
2013Deficient repair of ubiquitous errors in the genome risks faulty transcription or replication. Its direct and indirect phenotypic consequences are rare, complex, dementing, lethal disorders of children with inadequately understood overlapping genotypes and variable severity.
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Nucleotide excision repair and chromatin remodeling
European Journal of Biochemistry, 2002The organization of DNA within eukaryotic cell nuclei poses special problems and opportunities for the cell. For example, assembly of DNA into chromatin is thought to be a principle mechanism by which adventitious general transcription is repressed. However, access to genomic DNA for events such as DNA repair must be facilitated by energy‐intensive ...
Kiyoe, Ura, Jeffrey J, Hayes
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Protein complexes in nucleotide excision repair
Mutation Research/DNA Repair, 1999The main pathway by which mammalian cells remove DNA damage caused by UV light and some other mutagens is nucleotide excision repair (NER). The best characterised components of the human NER process are those proteins defective in the inherited disorder xeroderma pigmentosum (XP). The proteins known to be involved in the first steps of the NER reaction
S J, Araújo, R D, Wood
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Mammalian nucleotide excision repair
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, 1995L, Ma, J H, Hoeijmakers, A J, van der Eb
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Nucleotide excision repair and neurological diseases
DNA Repair, 2008This review will examine the known and postulated relationships between nucleotide excision repair (NER) and neurological diseases. We will begin with a description of NER and its subpathways: global genomic repair (GGR), transcription-coupled repair (TCR) and transcription domain-associated repair (DAR).
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Mammalian Nucleotide Excision Repair
1997Mammalian nucleotide excision repair and the analog process initiated in bacteria by (A)BC excinuclease share many basic biochemical steps including DNA damage recognition, dual incision, oligonucleotide excision, repair synthesis and ligation (see Fig. 5.1).
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