DNA excision repair
Open accessAbstract
In nucleotide excision repair DNA damage is removed through incision of the damaged strand on both sides of the lesion, followed by repair synthesis, which fills the gap using the intact strand as a template, and finally ligation. In prokaryotes the damaged base is removed in a 12-13 nucleotide (nt)-long oligomer; in eukaryotes including humans the damage is excised in a 24-32 nt-long fragment. Excision in Escherichia coli is accomplished by three proteins designated UvrA, UvrB, and UvrC. In humans, by contrast, 16 polypeptides including seven xeroderma pigmentosum (XP) proteins, the trimric replication protein A [RPA, human single-stranded DNA binding protein (HSSB)], and the multisubunit (7-10) general transcription factor TFIIH are required for the dual incisions. Transcribed strands are specifically targeted for excision repair by a transcription-repair coupling factor both in E. coli and in humans. In humans, excision repair is an important defense mechanism against the two major carcinogens, sunlight and cigarette smoke. Individuals defective in excision repair exhibit a high incidence of cancer while individuals with a defect in coupling transcription to repair suffer from neurological and skeletal abnormalities.
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XPA stabilizes the bubble and helps position XPF and XPG endonucleases for 5′ and 3′ incisions to excise a 24-32 bp oligonucleotide containing the damaged lesion.
“XPA stabilizes the bubble and helps in positioning XPF and XPG endonucleases for respective 5′ and 3′ incisions to excise out a 24–32 bp oligonucleotide containing damaged lesion.”
From ATR- and ATM-Mediated DNA Damage Response Is Dependent on Excision Repair Assembly during G1 but Not in S Phase of Cell Cycle (2016) · cites this paper as [11]
XPA stabilizes the bubble and helps position XPF and XPG endonucleases for incisions that excise a 24-32 bp oligonucleotide containing the lesion.
“XPA stabilizes the bubble and aids in positioning the XPF and XPG endonucleases for respective 5’ and 3’ incisions to excise out a 24-32 bp oligonucleotide containing damaged lesion.”
From NER initiation factors, DDB2 and XPC, regulate UV radiation response by recruiting ATR and ATM kinases to DNA damage sites (2013) · cites this paper as [10]
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- Authors
- Sancar, A.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Sancar, Aziz
- ORCID
- Sancar, Aziz
- Venue
- Annual Review of Biochemistry
- Publisher
- Annual Reviews
- Published
- 1996-06
- Volume
- 65
- Issue
- 1
- Pages
- 43-81
- ISSN
- 0066-4154 (ISSN-L)
- 1545-4509
- OpenAlex
- W2172916891
- Cited by
- 1,131
- References
- 1
- Citations by year
- 2026: 10 · 2025: 7 · 2024: 14 · 2023: 14 · 2022: 7 · 2021: 12 · 2020: 20 · 2019: 15 · 2018: 15 · 2017: 19 · 2016: 24 · 2015: 15 · 2014: 20 · 2013: 23 · 2012: 24
- FWCI
- 8.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- nucleotide excision repair, DNA damage, xeroderma pigmentosum, replication protein A, TFIIH, Escherichia coli, carcinogens, cancer susceptibility
- MeSH terms
- Animals, Cell Cycle, DNA Damage, DNA Repair, Escherichia coli, Humans, SOS Response, Genetics, Transcription, Genetic
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