ArticleBiochemistry research international2012
Role of p16(INK4A) in Replicative Senescence and DNA Damage-Induced Premature Senescence in p53-Deficient Human Cells.
Article in Biochemistry research international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 75 citations in OpenAlex.
- Cellular senescence and inflammageing: from mechanisms to senotherapeutic interventions.Biogerontology · 2026Review
- Differential miRNA expression during replicative senescence of dental pulp stem cells with potential for forensic age assessment.Scientific reports · 2026Article
- γ-Oryzanol Ameliorates Endothelial Replicative Senescence via Downregulation of SGLT2 Expression to Attenuate NADPH-Driven Oxidative Stress.Biomolecules & therapeutics · 2026Article
- Divergent roles of DNA methylation, TRIM28, and p53 surveillance in human embryonic and trophoblast stem cells.bioRxiv : the preprint server for biology · 2025Article
- Multiorgan transcriptomics in mice identifies immunoglobulin heavy constant mu (Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Senescence landscape in the liver following sepsis and senolytics as potential therapeutics.Aging cell · 2025Article
- Identification and characterization of senescent macrophages in renal allograft rejection: a cross-species MultiOmics study.Frontiers in immunology · 2025Article
- Characterisation of premature cell senescence in Alzheimer's disease using single nuclear transcriptomics.Acta neuropathologica · 2024Article
- Article
- Cellular senescence induction leads to progressive cell death via the INK4a-RB pathway in naked mole-rats.The EMBO journal · 2023Article
- Intratumor Heterogeneity and Treatment Resistance of Solid Tumors with a Focus on Polyploid/Senescent Giant Cancer Cells (PGCCs).International journal of molecular sciences · 2023Review
- Evaluation of the anticancer effect of telomerase inhibitor BIBR1532 in anaplastic thyroid cancer in terms of apoptosis, migration and cell cycle.Medical oncology (Northwood, London, England) · 2023Article
- IL-8 concurrently promotes idiopathic pulmonary fibrosis mesenchymal progenitor cell senescence and PD-L1 expression enabling escape from immune cell surveillance.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- A Selective ALDH1A3 Inhibitor Impairs Mesothelioma 3-D Multicellular Spheroid Growth and Neutrophil Recruitment.International journal of molecular sciences · 2023Article
- Mesenchymal stromal cell senescence in haematological malignancies.Cancer metastasis reviews · 2023Review
- Accelerated Senescence and Apoptosis in the Rat Liver during the Progression of Diabetic Complications.The Malaysian journal of medical sciences : MJMS · 2022Article
- p16 Represses DNA Damage Repair via a Novel Ubiquitin-Dependent Signaling Cascade.Cancer research · 2022Article
- Senolytic-Mediated Elimination of Head and Neck Tumor Cells Induced Into Senescence by Cisplatin.Molecular pharmacology · 2022Article
- Targeting of lactate dehydrogenase C dysregulates the cell cycle and sensitizes breast cancer cells to DNA damage response targeted therapy.Molecular oncology · 2022Article
- The functional impact of nuclear reorganization in cellular senescence.Briefings in functional genomics · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p16(INK4A) (hereafter p16) tumor suppressor is encoded by the INK4A/ARF locus which is among the most commonly dysregulated sequences in human cancer. By inhibiting cyclin-dependent kinases, p16 activates the G1-S checkpoint, and this response is often considered to be critical for establishing a senescence-like growth arrest. Not all studies support a universal role for p16 in senescence. Single-cell analysis of noncancerous human fibroblast cultures undergoing senescence as a function of culture age (replicative senescence) has revealed that p16 is not expressed in the majority (>90%) of cells that exhibit features of senescence (e.g., flattened and enlarged morphology coupled with senescence-associated β-galactosidase expression), ruling out a requirement for p16 in this process. In addition, ionizing radiation triggers premature senescence in human cancer cell lines that do not express p16. These observations are made with cells that express wild-type p53, a key mediator of the DNA damage response. In this paper, we examine the growing evidence suggesting a negative regulatory relationship between p16 and p53 and discuss recent reports that implicate a role for p16 in replicative senescence and ionizing radiation-induced premature senescence in human cells that lack wild-type p53 function.
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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.