ArticleOncogene2005
Induction of p19INK4d in response to ultraviolet light improves DNA repair and confers resistance to apoptosis in neuroblastoma cells.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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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
23 citing papers in PubMed, 54 citations in OpenAlex.
- Modulation of inflammasome components in patients with heart failure using oral nutritional supplements: investigating the molecular mechanisms beyond the clinical benefit.European journal of nutrition · 2026Trial
- CIP/KIP and INK4 families as hostages of oncogenic signaling.Cell division · 2024Review
- INK4 cyclin-dependent kinase inhibitors as potential prognostic biomarkers and therapeutic targets in hepatocellular carcinoma.Bioscience reports · 2022Article
- Review
- BOK promotes chemical-induced hepatocarcinogenesis in mice.Cell death and differentiation · 2018Article
- Oxidative stress-induced CREB upregulation promotes DNA damage repair prior to neuronal cell death protection.Molecular and cellular biochemistry · 2017Article
- Article
- Non-canonical functions of cell cycle cyclins and cyclin-dependent kinases.Nature reviews. Molecular cell biology · 2016Review
- Differential response of normal and malignant urothelial cells to CHK1 and ATM inhibitors.Oncogene · 2015Article
- Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation.Molecular and cellular biochemistry · 2015Article
- E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells.Cell cycle (Georgetown, Tex.) · 2015Article
- Role of p19ink4d in the pathogenesis of hearing loss.International journal of clinical and experimental pathology · 2015Article
- CDKN2D-WDFY2 is a cancer-specific fusion gene recurrent in high-grade serous ovarian carcinoma.PLoS genetics · 2014Article
- p19(INK4d) mRNA and protein expression as new prognostic factors in ovarian cancer patients.Cancer biology & therapy · 2013Article
- A network of transcription factors operates during early tooth morphogenesis.Molecular and cellular biology · 2013Article
- Chromatin relaxation-mediated induction of p19INK4d increases the ability of cells to repair damaged DNA.PloS one · 2013Article
- E2F1 induces p19INK4d, a protein involved in the DNA damage response, following UV irradiation.Molecular and cellular biochemistry · 2012Article
- CDK2 and PKA mediated-sequential phosphorylation is critical for p19INK4d function in the DNA damage response.PloS one · 2012Article
- The retroviral cyclin of walleye dermal sarcoma virus binds cyclin-dependent kinases 3 and 8.Virology · 2011Article
- E2F1-mediated upregulation of p19INK4d determines its periodic expression during cell cycle and regulates cellular proliferation.PloS one · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genetic instability driving tumorigenesis is fueled by DNA damage and by errors made by the DNA replication. Upon DNA damage the cell organizes an integrated response not only by the classical DNA repair mechanisms but also involving mechanisms of replication, transcription, chromatin structure dynamics, cell cycle progression, and apoptosis. In the present study, we investigated the role of p19INK4d in the response driven by neuroblastoma cells against DNA injury caused by UV irradiation. We show that p19INK4d is the only INK4 protein whose expression is induced by UV light in neuroblastoma cells. Furthermore, p19INK4d translocation from cytoplasm to nucleus is observed after UV irradiation. Ectopic expression of p19INK4d clearly reduces the UV-induced apoptosis as well as enhances the cellular ability to repair the damaged DNA. It is clearly shown that DNA repair is the main target of p19INK4d effect and that diminished apoptosis is a downstream event. Importantly, experiments performed with CDK4 mutants suggest that these p19INK4d effects would be independent of its role as a cell cycle checkpoint gene. The results presented herein uncover a new role of p19INK4d as regulator of DNA-damage-induced apoptosis and suggest that it protects cells from undergoing apoptosis by allowing a more efficient DNA repair. We propose that, in addition to its role as cell cycle inhibitor, p19INK4d is involved in maintenance of DNA integrity and, therefore, would contribute to cancer prevention.
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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.