ReviewThe Journal of investigative dermatology2015
Oxidative and energy metabolism as potential clues for clinical heterogeneity in nucleotide excision repair disorders.
Review in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 27 citations in OpenAlex.
- Type I interferon signaling defines a novel disease signature in xeroderma pigmentosum C human keratinocytes.Scientific reports · 2026Article
- Xenopus as a model system for studying pigmentation and pigmentary disorders.Pigment cell & melanoma research · 2025Review
- Xenopus: An in vivo model for studying skin response to ultraviolet B irradiation.Development, growth & differentiation · 2023Article
- Siblings with Cockayne Syndrome B Type III Presenting with Slowly Progressive Cerebellar Ataxia.Internal medicine (Tokyo, Japan) · 2023Article
- Xeroderma Pigmentosum C (XPC) Mutations in Primary Fibroblasts Impair Base Excision Repair Pathway and Increase Oxidative DNA Damage.Frontiers in genetics · 2020Article
- UVB-induced DHODH upregulation, which is driven by STAT3, is a promising target for chemoprevention and combination therapy of photocarcinogenesis.Oncogenesis · 2019Article
- Fibroblast activation and abnormal extracellular matrix remodelling as common hallmarks in three cancer-prone genodermatoses.The British journal of dermatology · 2019Observational
- Premature skin aging features rescued by inhibition of NADPH oxidase activity in XPC-deficient mice.The Journal of investigative dermatology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide excision repair (NER) is an important DNA repair pathway involved in the removal of a wide array of DNA lesions. The absence or dysfunction of NER results in the following distinct disorders: xeroderma pigmentosum (XP), Cockayne syndrome (CS), cerebro-oculo-facio-skeletal (COFS) syndrome, UV-sensitive syndrome (UVSS), trichothiodystrophy (TTD), or combined syndromes including XP/CS, XP/TTD, CS/TTD, and COFS/TTD. In addition to their well-characterized role in the NER signaling pathway, NER factors also seem to be important in biological processes that are not directly associated with DNA damage responses, including mitochondrial function and redox homeostasis. The potential causative role of these factors in the large clinical spectrum seen in NER diseases is discussed in this review.
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Identifiers
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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.