Transcriptional and Posttranslational Regulation of Nucleotide Excision Repair: The Guardian of the Genome against Ultraviolet Radiation
Open accessAbstract
Ultraviolet (UV) radiation from sunlight represents a constant threat to genome stability by generating modified DNA bases such as cyclobutane pyrimidine dimers (CPD) and pyrimidine-pyrimidone (6-4) photoproducts (6-4PP). If unrepaired, these lesions can have deleterious effects, including skin cancer. Mammalian cells are able to neutralize UV-induced photolesions through nucleotide excision repair (NER). The NER pathway has multiple components including seven xeroderma pigmentosum (XP) proteins (XPA to XPG) and numerous auxiliary factors, including ataxia telangiectasia and Rad3-related (ATR) protein kinase and RCC1 like domain (RLD) and homologous to the E6-AP carboxyl terminus (HECT) domain containing E3 ubiquitin protein ligase 2 (HERC2). In this review we highlight recent data on the transcriptional and posttranslational regulation of NER activity.
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The common feature of the aforementioned damage is strong perturbation of the DNA helix.
“The common feature of the aforementioned damage is certainly the strong perturbation of the DNA helix [88,89].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [89]
Prokaryotic NER is far poorer in terms of protein complexes involved in repair.
“Prokaryotic NER is far poorer in terms of protein complexes involved in repair.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [89]
NER removes a wide variety of damage such as bulky DNA adducts, ROS-damaged bases, and damage resulting from crosslinking agents.
“Furthermore, NER removes a wide variety of damage such as bulky DNA adducts, ROS-damaged bases, and damage resulting from crosslinking agents.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [89]
Humans possess only NER mechanism for repair of dipyrimidine DNA lesions.
“Humans possess only NER mechanism for the repair of dipyrimidine DNA lesions.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [89]
In both prokaryotes and eukaryotes, NER can be divided into steps: damage detection, damage verification, incision, excision, and repair synthesis and ligation.
“However, in both taxa, NER can be divided into several common steps: (a) damage detection, (b) damage verification, (c) incision, (d) excision, and (e) repair synthesis and ligation.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [89]
NER is the main UV-damage removal pathway both in prokaryotes and eukaryotes.
“Nucleotide excision repair (NER) is the main UV-damage removal pathway both in prokaryotes and eukaryotes.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [89]
Eukaryotic NER can be divided into global genomic NER (GG-NER) and transcription-coupled NER (TC-NER).
“Eukaryotic NER can be divided into global genomic NER (GG-NER) and transcription-coupled NER (TC-NER) [89].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [89]
Repair of damage both in GG-NER and TC-NER requires chromatin remodeling for enhanced access of pathway factors to existing damage.
“Repair of damage both in GG-NER and TC-NER requires chromatin remodeling for the enhanced access of pathway factors to existing damage.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [89]
The NER pathway in eukaryotes is tightly regulated by post-translational modifications and chromatin dynamics.
“Moreover the NER pathway in eukaryotes is tightly regulated by post-translational modifications and chromatin dynamics reviewed in [89,106,107,108,109].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [89]
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Autophagic UVRAG Promotes UV-Induced Photolesion Repair by Activation of the CRL4 DDB2 E3 Ligase
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p300/CBP acetyl transferases interact with and acetylate the nucleotide excision repair factor XPG
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Cdt2-mediated XPG degradation promotes gap-filling DNA synthesis in nucleotide excision repair
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Insulin and glucose regulate the expression of the DNA repair enzyme XPD
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BackgroundNDR1 modulates the UV-induced DNA-damage checkpoint and nucleotide excision repair
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Phototherapie und Karzinogenese
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Flagged first, then by citations
Cited by
Sorted by citations
Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies
Kciuk, M., Marciniak, B., Mojzych, M., & Kontek, R. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21197264 · Cited by 168 · see citing works
“Sci. 2020, 21, 7264 24 of 33 MCM7 DNA replication licensing factor 7 MDC1 Mediator of DNA damage checkpoint protein 1 MDM2 E3 ubiquitin-protein ligase MDM2 MM Malignant melanoma MMEJ Microhomology-mediated end-joining MRN MRE11-RAD50-NBS1 complexes mtDNA Mitochondrial DNA MTHF 5,10-methyl tetrahydrofolate NAD+ Nicotin…”
BackgroundInfluentialRoles of UVA radiation and DNA damage responses in melanoma pathogenesis
Khan, A. Q., Travers, J. B., & Kemp, M. G. (2018) · Environmental and Molecular Mutagenesis · doi:10.1002/em.22176 · Cited by 152 · see citing works
Targeting Mitochondrial Oxidative Stress to Mitigate UV-Induced Skin Damage
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DNA Oxidation and Excision Repair Pathways
Lee, T.-H., & Kang, T.-H. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20236092 · Cited by 116 · see citing works
Self-citationSkin Regenerative and Anti-Cancer Actions of Copper Peptides
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- Authors
- Park, J.-M., & Kang, T.-H.
- Affiliations
- Department of Biological Science, Dong-A University, Busan 49315, Korea
- Dong-A University (KR)
- Corresponding author
- Kang, Tae-Hong
- ORCID
- Kang, Tae-Hong
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2016-11-04
- Volume
- 17
- Issue
- 11
- Pages
- 1840
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC5133840
- OpenAlex
- W2546753643
- Cited by
- 44
- References
- 110
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 4 · 2022: 7 · 2021: 4 · 2020: 6 · 2019: 6 · 2018: 6 · 2017: 2
- FWCI
- 0.42
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Research Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Keywords
- nucleotide excision repair, ultraviolet radiation, genome stability, cyclobutane pyrimidine dimers, 6-4 photoproducts, ATR kinase, HERC2, post-translational regulation, transcriptional regulation, DNA repair, skin cancer
- MeSH terms
- Animals, Chromosomal Proteins, Non-Histone, DNA Damage, DNA Repair, Humans, Protein Processing, Post-Translational, Pyrimidine Dimers, Skin Neoplasms, Transcription, Genetic, Ultraviolet Rays, Xeroderma Pigmentosum, Signal Transduction, Protein Isoforms, Guanine Nucleotide Exchange Factors, Ubiquitin-Protein Ligases, Xeroderma Pigmentosum Group A Protein, Ataxia Telangiectasia Mutated Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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