ArticleProceedings of the National Academy of Sciences of the United States of America2003
Global genome repair is required to activate KIN17, a UVC-responsive gene involved in DNA replication.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Assessing the genetic estimates of the association between plasma caffeine and cancer risk through Mendelian randomization.European journal of nutrition · 2025Pooled it
- Kin17 promotes rDNA transcription, ribosomal biogenesis, and cortical lamination.EMBO reports · 2025Article
- DNA/RNA-binding protein KIN17 supports esophageal cancer progression via resolving noncanonical STING activation induced by R-loop.Signal transduction and targeted therapy · 2025Article
- KIN17 modulates the WNT/β-catenin pathway and epithelial mesenchymal transition in non-small cell lung cancer.Scientific reports · 2025Article
- Onvansertib and Navitoclax Combination as a New Therapeutic Option for Mucinous Ovarian Carcinoma.International journal of molecular sciences · 2025Article
- KIN17 functions in DNA damage repair and chemosensitivity by modulating RAD51 in hepatocellular carcinoma.Human cell · 2024Article
- Signatures of Adaptation and Purifying Selection in Highland Populations of Dasiphora fruticosa.Molecular biology and evolution · 2024Article
- Kin17 regulates proper cortical localization of Miranda in Drosophila neuroblasts by regulating Flfl expression.Cell reports · 2024Article
- Roles and regulatory mechanisms of KIN17 in cancers (Review).Oncology letters · 2023Review
- Evolution of Methyltransferase-Like (METTL) Proteins in Metazoa: A Complex Gene Family Involved in Epitranscriptomic Regulation and Other Epigenetic Processes.Molecular biology and evolution · 2021Article
- Kin17 knockdown suppresses the migration and invasion of cervical cancer cells through NF-κB-Snail pathway.International journal of clinical and experimental pathology · 2020Article
- Biophysical characterization and molecular phylogeny of human KIN protein.European biophysics journal : EBJ · 2019Article
- Green tea extract promotes DNA repair in a yeast model.Scientific reports · 2019Article
- Kin17 facilitates multiple double-strand break repair pathways that govern B cell class switching.Scientific reports · 2016Article
- Spectro-Fluor™ Technology for Reliable Detection of Proteins and Biomarkers of Disease: A Pioneered Research Study.Diagnostics (Basel, Switzerland) · 2014Article
- Expression of Kin17 promotes the proliferation of hepatocellular carcinoma cellsOncology letters · 2014Article
- A conserved KIN17 curved DNA-binding domain protein assembles with SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE7 to adapt Arabidopsis growth and development to limiting copper availability.Plant physiology · 2014Article
- The Arabidopsis KIN17 and its homolog KLP mediate different aspects of plant growth and development.Plant signaling & behavior · 2014Article
- Control and target gene selection for studies on UV-induced genotoxicity in whales.BMC research notes · 2013Article
- Whales use distinct strategies to counteract solar ultraviolet radiation.Scientific reports · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
UV light provokes DNA lesions that interfere with replication and transcription. These lesions may compromise cell viability and usually are removed by nucleotide excision repair (NER). In humans, inactivation of NER is associated with three rare autosomal recessive inherited disorders: xeroderma pigmentosum (XP), Cockayne syndrome, and trichothiodystrophy. The NER earliest step is lesion recognition by a complex formed by XPC and HHR23B proteins. In a subsequent step, XPA protein becomes associated to the repair complex. Here we investigate whether XPA and XPC proteins, involved in global genome repair, may contribute to a signal transduction pathway regulating the response to UVC-induced lesions. We monitored the expression of several UVC-induced genes in cells deficient in either a transduction pathway or mutated on an NER gene. Expression of the KIN17 gene is induced after UVC irradiation independently of p53 and of activating transcription factor 2. However, in human cells derived from XPA or XPC patients the UVC-induced accumulation of KIN17 RNA and protein is abolished. Our results indicate that the presence of functional XPA and XPC proteins is essential for the up-regulation of the KIN17 gene after UVC irradiation. They also show that the integrity of global genome repair is required to trigger KIN17 gene expression and probably other UVC-responsive genes.
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