The DOI matches its Crossref record; 82 of the 92 references it cites were found in a registry or an index.
The INK4A/ARF locus and its two gene products.
Abstract
The INK4A/ARF locus on chromosome 9 is one of the sites mutated most frequently in human cancer. Two genes comprising overlapping reading frames encoding p16(INK4a) and p19(ARF) have been discovered at this locus and, remarkably, both play an important role in regulating cell growth, survival and senescence.
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“In contrast, the biological action of Arf relies on the p53 pathway. This is because Arf can directly bind to mouse double minute 2 homolog (MDM2) and cause the accumulation of p53 by segregating MDM2 from p53 and by inhibiting MDM2’s E3 ubiquitin protein ligase activity for p53.10,11,14”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [11]
In the citing paper
“Therefore, activation of p53 by Arf can induce not only senescence but also apoptosis, depending on which gene downstream of p53 is induced after p53 activation.”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [11]
In the citing paper
“The p16-Arf locus encodes 2 tumor suppressors, p16 and Arf.10-12”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [11]
Citations
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“The Ink4a/Arf 4 locus encodes the tumor suppressors p16Ink4a (p16) and p19Arf (Arf) [214].”
BackgroundWalter, L. (2022) · Digital Archive @ GSU · doi:10.57709/11893597
Demidova, E. V., Iqbal, W., & Arora, S. (2018) · Current cancer research · doi:10.1007/978-3-319-78762-6_7
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“They are important regulators of retinoblastoma and p53 pathways, respectively, and upon activation produce growth arrest, senescence or apoptosis (Lowe and Sherr, 2003; Sharpless and DePinho, 1999).”
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Metadata
- Authors
- Sharpless, N. E., & DePinho, R. A.
- Affiliations
- Dana-Farber Cancer Institute (US)
- Corresponding author
- DePinho, Ronald A
- Venue
- Current Opinion in Genetics & Development
- Publisher
- Elsevier BV
- Published
- 1999-02
- Volume
- 9
- Issue
- 1
- Pages
- 22-30
- ISSN
- 0959-437X (ISSN-L)
- OpenAlex
- W1991595805
- Cited by
- 533
- References
- 92
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 8 · 2023: 7 · 2022: 10 · 2021: 15 · 2020: 8 · 2019: 9 · 2018: 11 · 2017: 4 · 2016: 12 · 2015: 9 · 2014: 12 · 2013: 21 · 2012: 15
- FWCI
- 5.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Genetics & Development (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hd028317-05, 7r01ey011267-04)
- National Eye Institute (R01EY11267)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01 HD28317)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- INK4a/ARF locus, p16INK4a, p19ARF, chromosome 9, tumor suppressor, cell cycle regulation, cellular senescence, cell growth, cell survival, cancer mutations
- MeSH terms
- Amino Acid Sequence, Humans, Molecular Sequence Data, Mutation, Neoplasms, Proteins, Genes, Tumor Suppressor, Sequence Homology, Amino Acid, Cyclin-Dependent Kinase Inhibitor p16, Genes, p16, Tumor Suppressor Protein p14ARF
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