The DOI matches its Crossref record; 54 of the 56 references it cites were found in a registry or an index.
Tumor suppression by Ink4a-Arf: progress and puzzles.
Abstract
The two products of the Ink4a-Arf locus, p16(Ink4a) and p19(Arf) (p14(ARF) in humans), are potent tumor suppressors that regulate the activities of the retinoblastoma protein and the p53 transcription factor. These proteins form part of a signaling network that is disrupted in most, if not all, cancer cells. The Ink4a-Arf locus responds to stress signals, limiting cell proliferation and modulating oncogene-induced apoptosis. Recent evidence emerging from mouse tumor models distinguishes the activities of p16(Ink4a) and p19(Arf) in regulating tumor onset and identifies differences in their responsiveness to drugs.
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In the citing paper
“Moreover, mutations that dampen the p53 or p16INK4a/pRB pathways confer resistance to senescence and greatly increase cancer risk [ 12 , 13 ].”
From Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor (2008) · cites this paper as [13]
In the citing paper
“In contrast, p16INK4a is poorly induced in senescent BJ fibroblasts and appears dispensable for senescence in MEFs (Beauséjour et al., submitted; Lowe and Sherr, 2003).”
From Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence (2003) · cites this paper as Lowe and Sherr, 2003
In the citing paper
“In contrast, p16INK4a is poorly induced in senescent BJ fibroblasts and appears dispensable for senescence in MEFs (Beauséjour et al., submitted; Lowe and Sherr, 2003).”
From Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence (2003) · cites this paper as Lowe and Sherr, 2003
In the citing paper
“p16 is induced by a variety of stressful stimuli, including overexpression of oncogenes such as RAS and suboptimal culture conditions (Lowe and Sherr, 2003).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Lowe and Sherr, 2003
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 [10]
In the citing paper
“p16 functions as a cyclin-dependent kinase (CDK) 4/6 inhibitor.10”
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 [10]
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 [10]
In the citing paper
“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 [10]
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Kisseljov, F. L., Мазуренко, Н. Н., Волгарева, Г. М., & Kisseljova, N. P. (2004) · Molecular Biology · doi:10.1023/b:mbil.0000023732.92750.ae · Cited by 3
“Loss of heterozygosity (LOH) is one of the markers of such alterations.”
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Su, H., Katz, S. G., & Slavoff, S. A. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.10.22.619581 · Cited by 4
“Expression of two different proteins from the same gene via alternative transcripts has previously been reported: for example, transcripts arising from alternative transcription start sites (TSS) in the CDKN2A gene encode INK4A and ARF, which share no amino acid sequence ( 12, 13 ).”
The ARF protein in tumor suppression: lessons from mouse models and human tumors
Rodríguez, I. P. (2004) · Clinical & Translational Oncology · doi:10.1007/bf02710031 · Cited by 2
Regulation of p53 Activity and Associated Checkpoint Controls
Post, S. M., Quintás‐Cardama, A., & Lozano, G. (2009) · Humana Press eBooks · doi:10.1007/978-1-60761-178-3_11 · Cited by 2
Unveiling CDKN2B-AS1: The functional long noncoding RNA driving age-related diseases
Chen, H., Huan, Q., Wang, Z., Cheng, W., Zhai, J., & Wu, G. (2025) · Gene Reports · doi:10.1016/j.genrep.2025.102247 · Cited by 3
Unraveling the Roles of Canonical and Noncanonical PRC1 Complexes
Conway, E., & Bracken, A. P. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-809737-3.00004-0 · Cited by 2
Pancreatic Progenitor Commitment Is Marked by an Increase in Ink4a/Arf Expression
Montano, E., Pollice, A., Lucci, V., Falco, G., Affinito, O., Mantia, G. L., Vivo, M., & Angrisano, T. (2021) · Biomolecules · doi:10.3390/biom11081124 · Cited by 3
“While p16Ink4a and p19Arf induction in cultured primary cells cause senescence [30], Bmi-1 overexpression can prevent senescence and extend their replicative lifespan by reducing p16Ink4a and p19Arf expression [31].”
BackgroundOvercoming Resistance to BRAF and MEK Inhibitors by Simultaneous Suppression of CDK4
Dong, J. (2013) · InTech eBooks · doi:10.5772/53620 · Cited by 2
“p16 binds to and inhibits the catalytic activity of CDK4, representing a crucial gatekeeper at the G1>S checkpoint [62, 63].”
BackgroundCancer Stem-Cell Related miRNAs: Novel Potential Targets for Metastatic Prostate Cancer
Singh, A. N., Khandwekar, A. P., & Sharma, N. (2015) · Journal of Analytical Oncology · doi:10.6000/1927-7229.2015.04.04.4 · Cited by 2
Piersigilli, A., Borowsky, A., Chen, Q., Hubbard, N. E., & Cardiff, R. D. (2015) · Journal of Analytical Oncology · doi:10.6000/1927-7229.2015.04.04.8 · Cited by 2
Brown, N. E., & Hinds, P. W. (2015) · Elsevier eBooks · doi:10.1016/b978-1-4557-4066-6.00003-2 · Cited by 2
Mouse models of human B lymphoid neoplasms
Herbert C. Morse III, J. M. W. A. M. A. T. (2010) · CRC Press eBooks · doi:10.1201/b13424-26 · Cited by 2
Волгарева, Г. М. (2020) · Russian Journal of Biotherapy · doi:10.17650/1726-9784-2020-19-3-6-11 · Cited by 2
Ai, Y., Sakamuru, S., Imler, G. H., Xia, M., & Xue, F. (2022) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2022.116890 · Cited by 2
Modifiers of Neural Stem Cells and Aging: Pulling the Trigger of a Neurogenic Decline
Nivet, E. (2016) · Current Stem Cell Reports · doi:10.1007/s40778-016-0047-3 · Cited by 2
Zhao, F., Guo, J., Cui, K., & Xiong, S. (2006) · Infectious Diseases in Clinical Practice · doi:10.1097/01.idc.0000210288.53893.50 · Cited by 2
Cell Cycle Control and Dysregulation Protocols
Giordano, A., & Romano, G. (2004) · Humana Press eBooks · doi:10.1385/1592598226 · Cited by 2
Fine, R. L., Mao, Y., García‐Carracedo, D., Su, G. H., Qiu, W., HOCHFELD, U., NICHOLS, G. L., Li, Y., Dinnen, R. D., Raffo, A. J., et al. (2023) · Biomedicines · doi:10.3390/biomedicines11020258 · Cited by 1
Kurayoshi, K., Tanaka, M., Nakajima, R., Zhou, Y., Shirasawa, M., Fikriyanti, M., Fujisawa, J.-I., Iwanaga, R., Bradford, A. P., Araki, K., et al. (2025) · Cells · doi:10.3390/cells14241953 · Cited by 2
Cellular Senescence and Its Relation with Telomere
Arenas-Aranda, D. J., Hernández-Caballero, M. E., & Salamanca‐G�mez, F. (2012) · InTech eBooks · doi:10.5772/32949 · Cited by 1
The Role of MicroRNAs in Regulating Cancer Stem Cells
Tuna, M., & Christopher, I. L. (2011) · InTech eBooks · doi:10.5772/24822 · Cited by 1
“For example, the p53, PTEN, and INK4A pathways are involved in stem cell self-renewal (Armesilla-Diaz et al., 2009b; Cicalese et al., 2009; Lowe and Sherr, 2003; Nagao et al., 2008; Zheng et al., 2008a) (Table 1).”
BackgroundGamma Radiation Induces p53-Mediated Cell Cycle Arrest in Bone Marrow Cells
Moraes, A. A. F. S., Lucimar, P., Vanina, M., Lasakosvitsch, F., Gaiba, S., Azevedo, F. L. A., Amanda, P. A., Segreto, H. R. C., Alice, T., & Jeronimo, P. (2012) · InTech eBooks · doi:10.5772/38522 · Cited by 1
Targeting the p53 tumor suppressor gene function in glioblastomas using small chemical molecules
Magrini, R., Bakker, A. C., Gaviraghi, G., & Terstappen, G. C. (2006) · Drug Development Research · doi:10.1002/ddr.20151 · Cited by 1
“…mechanisms, one of which is to target p53 to the proteasome degradation system [Haupt et al., 1997; Kubbutat et al., 1997]. p14ARF, encoded by the INK4/ARF locus, binds and sequesters hdm2 in the nucleolus [Lowe and Sherr, 2003], thus enabling p53 to be released from its negative regulator.”
Metabolic Enzymes: The Novel Targets for Cancer Stem Cells
Li, J. L. P. (2014) · Journal of Stem Cell Research & Therapy · doi:10.4172/2157-7633.1000197 · Cited by 1
“The fact that many key genes are involved in both CSCs proliferation and normal stem cells regulation through various pathways such as Wnt/β-catenin [5], Hedgehog [6], Bim-1 [7,8], p53, p16INK4a and p19ARF [9], has made it more important to identify genes that are functionally required by CSCs but not by normal stem c…”
BackgroundHerrera-Merchan, A., Hidalgo, I., Arranz, L., & González, S. (2012) · InTech eBooks · doi:10.5772/32121 · Cited by 1
“Through the activation of Rb and p53, the INK4/ARF locus is able to induce cell senescence and cell death (Gil and Peters, 2006; Lowe and Sherr, 2003).”
BackgroundGuo, J. C., Feng, Y., & Li, H. (2016) · Journal of Hypertension Open Access · doi:10.4172/2167-1095.1000233 · Cited by 1
“These genes involved in the regulation of the cell cycle and would be implicated, and transform growth factor (TGF)--induced growth inhibition, in the pathogenesis of atherosclerosis [16-19].”
BackgroundPathogenesis of T-Non-Hodgkin’s Lymphoma
Bond, J., & Smith, O. P. (2019) · Springer eBooks · doi:10.1007/978-3-030-11769-6_5 · Cited by 1
Ullah, I., Lee, R., Oh, K. B., Kim, Y.-I., Woo, J.-S., Hwang, S., Im, G., & Ock, S. A. (2019) · Transplantation Proceedings · doi:10.1016/j.transproceed.2019.03.028 · Cited by 1
Molecular genetics and mechanisms of pigmentation and melanoma
Sundström, E. (2010) · Epsilon Open Archive (Sveriges lantbruksuniversitet biblioteket (Swedish University of Agricultural Sciences)) · Cited by 1
Darbro, B. W. (2007) · doi:10.17077/etd.2qnj4kik · Cited by 1
González-Cano, L. (2013) · Dialnet (Universidad de la Rioja) · Cited by 1
Metadata
- Authors
- Lowe, S. W., & Sherr, C. J.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- St. Jude Children's Research Hospital (US)
- Corresponding author
- Lowe, Scott W
- Sherr, Charles J
- Venue
- Current Opinion in Genetics & Development
- Publisher
- Elsevier BV
- Published
- 2003-02
- Volume
- 13
- Issue
- 1
- Pages
- 77-83
- ISSN
- 0959-437X (ISSN-L)
- OpenAlex
- W1984948591
- Cited by
- 699
- References
- 56
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 3 · 2023: 20 · 2022: 10 · 2021: 5 · 2020: 10 · 2019: 15 · 2018: 10 · 2017: 17 · 2016: 17 · 2015: 29 · 2014: 30 · 2013: 48 · 2012: 34
- FWCI
- 6.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Genetics & Development (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Funders
- National Cancer Institute (P30CA008748)
- 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 › PI3K/AKT/mTOR signaling in cancer
- Keywords
- INK4a/ARF locus, p16INK4a, p19ARF, tumor suppression, retinoblastoma protein, p53, stress signaling, cell proliferation, tumor onset, mouse tumor model, drug response
- MeSH terms
- Animals, Humans, Lymphoma, Neoplasms, Tumor Suppressor Protein p53, Retinoblastoma Protein, Cyclin-Dependent Kinase Inhibitor p16, ADP-Ribosylation Factors, Feedback, Physiological, Mice, Rats
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