ReviewNature reviews. Molecular cell biology2006
Regulation of the INK4b-ARF-INK4a tumour suppressor locus: all for one or one for all.
Review in Nature reviews. Molecular cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 463 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
463 citing papers in PubMed, 2 syntheses or guidelines pooled it, 818 citations in OpenAlex.
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- MTAP Deficiency as a Metabolic Vulnerability in Cancer: Implications for Synthetic Lethal Therapy.Cancer science · 2026Review
- Frequent expression of aberrant chimeric Cdkn2a transcripts in mouse models of muscular dystrophy.Scientific reports · 2026Article
- Therapeutic vulnerabilities exposed by the 9p21 loss identified through multiparametric drug screening inform rational combination strategies.NPJ precision oncology · 2026Article
- Review
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- Biomarkers of Common Molecular Dysregulation in Tumor Tissue and Peritumor Mucosa in Head and Neck SCC: Insights into Field Cancerization.International journal of molecular sciences · 2026Review
- G1/S arrest: a key mechanism of cellular aging and replicative senescence.Biogerontology · 2026Review
- Senescence-associated and immune-related 9p21.3 locus genes in colorectal cancer: epigenetic architecture, molecular landscape and therapeutic possibilities.Frontiers in cell and developmental biology · 2026Review
- High-Risk neuroblastoma therapeutics Topotecan and 13-cis-Retinoic acid modulate autophagy and induce DNA damage response in hematopoietic stem cells and monocytes.Scientific reports · 2025Article
- Enhancer-targeting CRISPR screens at coronary artery disease loci suggest shared mechanisms of disease risk.medRxiv : the preprint server for health sciences · 2025Article
- Hallmarks and mechanisms of cellular senescence in aging and disease.Cell death discovery · 2025Review
- Interpreting the Origins and Functions of Noncoding RNAs From the Ribosomal Genes.Journal of cellular physiology · 2025Review
- Hallmarks of cellular senescence: biology, mechanisms, regulations.Experimental & molecular medicine · 2025Review
- EBV Latency Programs: Molecular and Epigenetic Regulation and Its Role in Disease Pathogenesis.Journal of medical virology · 2025Review
- Craniomaxillofacial-Derived MSCs in Congenital Defect Reconstruction.Biomolecules · 2025Review
- Preventing MSC aging and enhancing immunomodulation: Novel strategies for cell-based therapies.Regenerative therapy · 2025Review
403 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The INK4b-ARF-INK4a locus encodes two members of the INK4 family of cyclin-dependent kinase inhibitors, p15(INK4b) and p16(INK4a), and a completely unrelated protein, known as ARF. All three products participate in major tumour suppressor networks that are disabled in human cancer and influence key physiological processes such as replicative senescence, apoptosis and stem-cell self-renewal. Transcription from the locus is therefore kept under strict control. Mounting evidence suggests that although the individual genes can respond independently to positive and negative signals in different contexts, the entire locus might be coordinately suppressed by a cis-acting regulatory domain or by the action of Polycomb group repressor complexes.
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Identifiers
What OpenQuestion holds
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.