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]
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“gif" NDATA ITEM> ]> The cyclin-dependent kinase inhibitor p16 INK4a can induce senescence of human cells, and its loss by deletion, mutation or epigenetic silencing is among the most frequently observed molecular lesions in human cance”
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ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage
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“Although most mutations at the CDKN2A locus found in human tumours result in disruption of both the ARF and INK4A transcripts, the presence of point mutations and small deletions that specifically affect p16 INK4a strongly implicate p16 INK4a as a tumour suppresso”
BackgroundUV-induced DNA damage, repair, mutations and oncogenic pathways in skin cancer
de Gruijl, F. R., van Kranen, H. J., & Mullenders, L. H. F. (2001) · Journal of Photochemistry and Photobiology B Biology · doi:10.1016/s1011-1344(01)00199-3 · Cited by 549
'Super p53' mice exhibit enhanced DNA damage response, are tumor resistant and age normally
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Cancer and ageing: rival demons?
Campisi, J. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1073 · Cited by 512
p16(MTS-1/CDKN2/INK4a) in Cancer Progression
Rocco, J. W., & Sidransky, D. (2001) · Experimental Cell Research · doi:10.1006/excr.2000.5149 · Cited by 471
“In a recent reanalysis of 714 primary tumors and cell lines in which the status of p14, p16, and p53 could be reasonably inferred, the authors concluded that the role for p14 in human malignancy appeared to be minor [91].”
BackgroundResultInfluentialNucleolus, Ribosomes, and Cancer
Montanaro, L., Treré, D., & Derenzini, M. (2008) · American Journal Of Pathology · doi:10.2353/ajpath.2008.070752 · Cited by 456
“The activity of p53 may also be influenced by changes in the expression of p14Arf, the tumor suppressor protein encoded by the Arf gene located in the Ink4a-Arf locus.(49) The Arf gene is induced by a series of stress signals such as hyperproliferative signals emanating from oncogenic Ras and overexpressed Myc and may…”
BackgroundINK4a/ARF: A multifunctional tumor suppressor locus
Sharpless, N. E. (2005) · Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis · doi:10.1016/j.mrfmmm.2004.08.021 · Cited by 442
Self-citationBmi1, stem cells, and senescence regulation
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Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency
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“The Cdkn2a locus encodes two separate tumour suppressors, p16 Ink4a , a cyclin-dependent kinase (Cdk) inhibitor that can block G 1 –S progression when present above a certain level, and p19 Arf , a positive regulator of the transcription factor p53 that integrates and responds to a wide variety of cellular stresse”
The power and the promise of oncogene-induced senescence markers
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“These two pathways are thought to be crucial for tumour suppression and are often mutated in tumour”
BackgroundReactive Oxygen Species in Normal and Tumor Stem Cells
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“…retinoblastoma protein (Rb) hypophosphorylation and suppresses the expression of E2F-dependent genes, resulting in restriction of G1/S cell cycle progression and formation of senescence-associated heterochromatic foci (SAHF) (Lowe & Sherr, 2003; Narita et al., 2003; Sharpless & DePinho, 1999).”
BackgroundNUMB controls p53 tumour suppressor activity
Colaluca, I. N., Tosoni, D., Nuciforo, P., Senic-Matuglia, F., Galimberti, V., Viale, G., Pece, S., & Di Fiore, P. P. (2008) · Nature · doi:10.1038/nature06412 · Cited by 385
Cell cycle checkpoints and their inactivation in human cancer
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“A more accurate mapping of the INK4a locus has shown that it also encodes another protein, called p19ARF, which has a role in regulating p53 stability and which is frequently found to be mutated in cancer (Roussel 1999; Sharpless & DePinho 1999).”
BackgroundAlterations of the Notch pathway in lung cancer
Westhoff, B., Colaluca, I. N., D’Ario, G., Donzelli, M., Tosoni, D., Volorio, S., Pelosi, G., Spaggiari, L., Mazzarol, G., Viale, G., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0907781106 · Cited by 388
Translating p53 into the clinic
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“Similarly, methylation at the CDKN2A ( INK4a/ARF ) locus can epigenetically silence the expression of the p14ARF protein, and block the ability of activated oncogenes to stabilize the p53 response”
BackgroundDAP kinase activates a p19ARF/p53-mediated apoptotic checkpoint to suppress oncogenic transformation
Raveh, T., Droguett, G., Horwitz, M. S., DePinho, R. A., & Kimchi, A. (2001) · Nature Cell Biology · doi:10.1038/35050500 · Cited by 361
“Among the various mechanisms that activate p53, a role for p19 ARF has been established in which it stabilizes p53 by binding to Mdm2 and preventing p53 degradatio”
BackgroundSelf-citationTotal body irradiation selectively induces murine hematopoietic stem cell senescence.
Wang, Y., Schulte, B. A., LaRue, A. C., Ogawa, M., & Zhou, D. (2006) · Blood · doi:10.1182/blood-2005-04-1418 · Cited by 351
Naive T Cell Maintenance and Function in Human Aging
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“The INK4A/ARF locus comprises overlapping reading frames of two genes, p16 and p19, that play important roles as cell cycle inhibitors in regulating cell growth and senescence and are mutated in various forms of cancer (74, 75).”
BackgroundPolycomb CBX7 has a unifying role in cellular lifespan.
Gil, J., Bernard, D., Martínez, D., & Beach, D. (2004) · Nature Cell Biology · doi:10.1038/ncb1077 · Cited by 341
“Both p16 Ink4a and Arf are mutated in a high percentage of human cancer”
Hematopoietic Stem Cell Injury Induced by Ionizing Radiation
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“Once SAHF are formed after the engagement of the p16-Rb pathway, the cells become permanently growth arrested and senescent.”
InfluentialA pivotal role for ERK in the oncogenic behaviour of malignant melanoma?
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Cyclin-Dependent Kinase Inhibitors: Useful Targets in Cell Cycle Regulation
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The INK4 family of cell cycle inhibitors in cancer
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“Several excellent reviews on CKIs (Harper and Elledge, 1996; Nakayama and Nakayama, 1998) and the roles of p16INK4a (Ruas and Peters, 1998) and the INK4a/ARF locus in cancer have been recently published (Sherr, 1998; Sharpless and DePinho, 1999).”
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“Ink4a and Arf are important players in the retinoblastoma (pRB) and p53 pathways, respectively, and their activation results in growth arrest, senescence, or apoptosis (for review, see Sharpless and DePinho 1999; Lowe and Sherr 2003).”
BackgroundJacobs, J. J. L., Keblusek, P., Robanus-Maandag, E., Kristel, P., Lingbeek, M., Nederlof, P. M., van Welsem, T., van de Vijver, M. J., Koh, E. Y., Daley, G. Q., et al. (2000) · Nature Genetics · doi:10.1038/81583 · Cited by 368
“CDKN2A (p16 INK4a ) is encoded by the CDKN2A ( INK4a/ARF ) tumour suppressor locu”
BackgroundSenescent Cells: A Novel Therapeutic Target for Aging and Age-Related Diseases
Naylor, R. M., Baker, D. J., & van Deursen, J. M. (2012) · Clinical Pharmacology & Therapeutics · doi:10.1038/clpt.2012.193 · Cited by 288
Cooperative Signals Governing ARF-Mdm2 Interaction and Nucleolar Localization of the Complex
Weber, J. D., Kuo, M.-L., Bothner, B. B., DiGiammarino, E. L., Kriwacki, R. W., Roussel, M. F., & Sherr, C. J. (2000) · Molecular and Cellular Biology · doi:10.1128/mcb.20.7.2517-2528.2000 · Cited by 275
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Self-citationThe INK4a/ARF locus and melanoma
Sharpless, N. E., & Chin, L. (2003) · Oncogene · doi:10.1038/sj.onc.1206461 · Cited by 260
“…locus encodes two distinct proteins, p16INK4a and p14ARF (p19ARF in the mouse), both of which demonstrate tumor suppressor activity in genetically distinct anticancer pathways (i.e. the ‘Rb pathway’ for p16INK4a and the ‘p53 pathway’ for p14ARF) (Ruas and Peters, 1998; Sharpless and DePinho, 1999).”
BackgroundSelf-citationLinggi, B. E., Müller‐Tidow, C., van de Locht, L. T., Hu, M., Nip, J., Serve, H. L., Berdel, W. E., van der Reijden, B., Quelle, D. E., Rowley, J. D., et al. (2002) · Nature Medicine · doi:10.1038/nm726 · Cited by 261
“Therefore, these mRNAs encode two proteins that share identical nucleotide sequence within the second exon, but each has unique coding potentia”
BackgroundAge to survive: DNA damage and aging
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Stabilization of p53 by p14ARF without relocation of MDM2 to the nucleolus
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Cellular Senescence: Molecular Mechanisms, In Vivo Significance, and Redox Considerations
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“Although substantial progress has been made in our understanding of the molecular mechanisms underlying senescence (51, 390, 392, 394, 451), a good deal of uncertainty remains as to the in vivo relevance of senescence and the role it plays in the normal aging process and various pathologic…”
Cell proliferation and apoptosis
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“This results in activation of the p53 target genes involved in cell cycle arrest, apoptosis, or senescence (10).”
INK4a‐deficient human diploid fibroblasts are resistant to RAS‐induced senescence
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Role of p14ARF in Replicative and Induced Senescence of Human Fibroblasts
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“This line of reasoning agrees with our observations that Arf, the expression of which is known to respond to signaling imbalances (60), but not DNA damage (65) or oxidative stress (15), is upregulated in senescent rodent cultures but not human cultures.”
ResultSaheb-Al-Zamani, M., Yan, Y., Farber, S. J., Hunter, D. A., Newton, P., Wood, M. D., Stewart, S. A., Johnson, P. J., & Mackinnon, S. E. (2013) · Experimental Neurology · doi:10.1016/j.expneurol.2013.04.011 · Cited by 213
“However, each pathway, while distinct, shares many similar features including triggers and intermediate factors making them difficult to separate (Campisi and d'Adda di Fagagna, 2007; Serrano and Blasco, 2001; Sharpless and DePinho, 1999).”
BackgroundWang, Y., Probin, V., & Zhou, D. (2006) · Current Cancer Therapy Reviews · doi:10.2174/157339406777934717 · Cited by 217
“Activation of Erk/p38 MAPK appears to act downstream of Ras [38,75].”
BackgroundInfluentialTranslational Repression of C. elegans p53 by GLD-1 Regulates DNA Damage-Induced Apoptosis
Schumacher, B., Hanazawa, M., Lee, M., Nayak, S., Volkmann, K., Hofmann, R., Hengartner, M. O., Schedl, T., & Gartner, A. (2005) · Cell · doi:10.1016/j.cell.2004.12.009 · Cited by 221
“Although human cancers commonly contain mutations in the p53 gene itself, many of the remaining tumors have defects in upstream signaling components of the p53 pathway such as inactivation of the positive regulators ARF or CHK2 (Sharpless and DePinho, 1999; Bartek and Lukas, 2003), or overexpression of the negative re…”
BackgroundHuman melanocyte senescence and melanoma susceptibility genes
Bennett, D. C. (2003) · Oncogene · doi:10.1038/sj.onc.1206446 · Cited by 220
“…melanoma susceptibility in humans is found on chromosome 9p21 and is known variously as cyclin-dependent kinase inhibitor 2A (CDKN2A), multiple tumor suppressor 1 (MTS1) or INK4A-ARF (for reviews, see Ruas and Peters, 1998; Sharpless and DePinho, 1999; Hayward, 2000; Rocco and Sidransky, 2001).”
BackgroundBmi1 Is a Key Epigenetic Barrier to Direct Cardiac Reprogramming
Zhou, Y., Wang, L., Vaseghi, H. R., Liu, Z., Lu, R., Alimohamadi, S., Yin, C., Fu, J., Wang, G. G., Liu, J., et al. (2016) · Cell stem cell · doi:10.1016/j.stem.2016.02.003 · Cited by 209
“Based on previous reports that Bmi1 and its downstream targets are involved in cell proliferation and senescence (Jacobs et al., 1999; Levine, 1997; Quelle et al., 1995; Sharpless and DePinho, 1999), we sought to determine the requirement of cell proliferation in shBmi1-mediated iCM reprogramming.”
Wide spectrum of tumors in knock‐in mice carrying a Cdk4 protein insensitive to INK4 inhibitors
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“Increased expression of p16 has been widely used as a senescence biomarker and it also functions as an important mediator of cellular senescence induction [24, 25].”
BackgroundDamalas, A., Kahan, S., Shtutman, M. S., Ben‐Ze'ev, A., & Oren, M. (2001) · The EMBO Journal · doi:10.1093/emboj/20.17.4912 · Cited by 208
DNA methylation in breast cancer.
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“. These two transcripts share identical second and third exons but have distinct first exons ( Sharpless & DePinho 1999 ).”
Fiore, R. D., D’Anneo, A., Tesoriere, G., & Vento, R. (2013) · Journal of Cellular Physiology · doi:10.1002/jcp.24329 · Cited by 211
Reactive oxygen species and hematopoietic stem cell senescence
Shao, L., Li, H., Pazhanisamy, S. K., Meng, A., Wang, Y., & Zhou, D. (2011) · International Journal of Hematology · doi:10.1007/s12185-011-0872-1 · Cited by 205
“HSCs from Bmi1−/− mice express increased levels of p16 and Arf [27, 57, 58].”
BackgroundInfluentialDNA methylation in hepatocellular carcinoma
Tischoff, I. (2008) · World Journal of Gastroenterology · doi:10.3748/wjg.14.1741 · Cited by 193
Meng, A., Wang, Y., Zant, G. E. V., & Zhou, D. (2003) · PubMed · Cited by 193
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“…fact that most human cancers evolve ways to evade p53 tumor suppressor activity by selecting for mutations in p53 itself, inactivating upstream signaling components (Bartek and Lukas, 2003; Sharpless and DePinho, 1999), or over-expressing negative regulators such as Mdm2 (Freedman et al., 1999).”
The epistemic goal of a concept: accounting for the rationality of semantic change and variation
Brigandt, I. (2009) · Synthese · doi:10.1007/s11229-009-9623-8 · Cited by 189
“…DNA elements code for a product, such as RNA editing and translational recoding (Gray 2003; Baranov et al. 2003), overlapping genes (Mottus et al. 1997), transcription in different reading frames (Sharpless and DePinho 1999), and antisense transcription (Dorn and Krauss 2003; Yelin et al. 2003).”
BackgroundTransient Inactivation of Rb and ARF Yields Regenerative Cells from Postmitotic Mammalian Muscle
Pajcini, K. V., Corbel, S. Y., Sage, J., Pomerantz, J. H., & Blau, H. M. (2010) · Cell stem cell · doi:10.1016/j.stem.2010.05.022 · Cited by 193
“In marked contrast, in similar experiments using primary muscle cells isolated directly from mammalian muscle tissues, Rb reduction or elimination by Cre-mediated excision, failed to result in significant S-phase reentry (Sacco et al. 2003; Camarda et al. 2004; Huh et al. 2004).”
BackgroundResultMolecular markers in oral epithelial dysplasia: review
Pitiyage, G. N., Tilakaratne, W. M., Tavassoli, M., & Warnakulasuriya, S. (2009) · Journal of Oral Pathology and Medicine · doi:10.1111/j.1600-0714.2009.00804.x · Cited by 185
p16Ink4a in Melanocyte Senescence and Differentiation
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Control of p53 ubiquitination and nuclear export by MDM2 and ARF.
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Epigenetic Control of a Transcription Factor at the Cross Section of Two Antagonistic Pathways
Álvarez-Venegas, R., Al-Abdallat, A. M., Guo, M., Alfano, J. R., & AVRAMOVA, Z. V. (2007) · Epigenetics · doi:10.4161/epi.2.2.4404 · Cited by 176
The human cytochrome P450 3A locus. Gene evolution by capture of downstream exons
Finta, C., & Zaphiropoulos, P. G. (2000) · Gene · doi:10.1016/s0378-1119(00)00470-4 · Cited by 169
p19ARF targets certain E2F species for degradation
Martelli, F., Hamilton, T., Silver, D. P., Sharpless, N. E., Bardeesy, N. M., Rokas, M., DePinho, R. A., Livingston, D. M., & Grossman, S. R. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.081061398 · Cited by 167
Self-citationShao, L., Feng, W., Li, H., Gardner, D., Luo, Y., Wang, Y., Liu, L., Meng, A., Sharpless, N. E., & Zhou, D. (2014) · Blood · doi:10.1182/blood-2013-07-515619 · Cited by 165
“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) Therefore, activation of p53 by Arf can induce not only senescence but also apoptosis, depending…”
BackgroundSelf-citationGenetically defined mouse models that mimic natural aspects of human prostate cancer development.
Roy‐Burman, P., Wu, H., Powell, W. C., Hagenkord, J. M., & Cohen, M. B. (2004) · Endocrine Related Cancer · doi:10.1677/erc.0.0110225 · Cited by 164
“The first transgenic mouse line, designed with the anticipation to induce prostate cancer, used a potentially prostate-restricted promoter, that is of the prostate steroid-binding protein C3(1) gene to drive expression of the SV40 viral large T-antigen (Maroulakou et al. 1994, Shibata et al. 1998).”
Dual Inactivation of RB and p53 Pathways in RAS-Induced Melanomas
Bardeesy, N., Bastian, B. C., Hezel, A., Pinkel, D., DePinho, R. A., & Chin, L. (2001) · Molecular and Cellular Biology · doi:10.1128/mcb.21.6.2144-2153.2001 · Cited by 166
“in the absence of germ line ARF-specific mutations in cancerprone kindreds (50).”
BackgroundSelf-citationInvasive melanoma in Cdk4-targeted mice
Sotillo, R., García, J. F., Ortega, S., Martín‐Broto, J., Dubus, P. R., Barbacid, M., & Malumbres, M. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.241338598 · Cited by 164
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“…upregulation and p16 INK4a mutation p16 INK4a regulates not only cell proliferation (Hayward, 2000; Rocco and Sidransky, 2001; Ruas and Peters, 1998; Sharpless and DePinho, 1999), but also the activity of the retinoblastoma (RB) protein family members, which are tumor suppressors and inhibitors of…”
BackgroundConstitutive and inducible expression and regulation of vascular endothelial growth factor
Xie, K., Wei, D., Shi, Q., & Huang, S. (2004) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2004.04.003 · Cited by 167
“p16 The Ink4a/Arf4 locus encodes the tumor suppressors p16Ink4a (p16) and p19Arf (Arf) [214].”
BackgroundÁlvarez-Venegas, R., Sadder, M. T., Hlavačka, A., Baluška, F., Xia, Y., Lu, G., Firsov, A., Sarath, G., Moriyama, H., DUBROVSKY, J. G., et al. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0600944103 · Cited by 161
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“Several studies have established that loss of p16 function can be an early event in tumor progression (42, 43) and that it is associated with tumor development (29, 44, 45).”
BackgroundSuppression of p53 by Notch in lymphomagenesis: implications for initiation and regression
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“pathway acts as a tumor surveillance mechanism that is activated in response to inappropriately sustained proliferative signals (21, 22).”
BackgroundCellular Response to Oncogenic Ras Involves Induction of the Cdk4 and Cdk6 Inhibitor p15INK4b
Malumbres, M., de Castro, I. P., Hernández, M. I., Jiménez, M., Corral, T., & Pellicer, À. (2000) · Molecular and Cellular Biology · doi:10.1128/mcb.20.8.2915-2925.2000 · Cited by 160
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Role of Polycomb Group Proteins in Stem Cell Self-Renewal and Cancer
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“Whereas p16 Ink4a is a cyclin-dependent kinase inhibitor that activates the Rb pathway through inhibition of cyclin D-Cdk4/6 complexes, Arf induces the p53 pathway by inhibiting Mdm2 function (Sharpless and DePinho, 1999; Sherr, 2001).”
p 21WAF1 C ontrol of E pithelial C ell C ycle and C ell F ate
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Promoter hypermethylation: a common cause of reduced p16(INK4a) expression in uveal melanoma.
van der Velden, P. A., Metzelaar-Blok, J. A. W., Bergman, W., Monique, H., Hurks, H. M. H., Frants, R. R., Gruis, N. A., & Jager, M. J. (2001) · PubMed · Cited by 147
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Genetic analysis of Pten and Ink4a/Arf interactions in the suppression of tumorigenesis in mice
You, M. J., Castrillón, D. H., Bastian, B. C., O’Hagan, R. C., Bosenberg, M., Parsons, R. E., Chin, L., & DePinho, R. A. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.022632099 · Cited by 143
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Alterations of p16(INK4a) and p14(ARF) in patients with severe oral epithelial dysplasia.
Kresty, L. A., Mallery, S. R., Knobloch, T. J., Song, H., Lloyd, M., Casto, B. C., & Weghorst, C. M. (2002) · PubMed · Cited by 142
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“More frequent cancer-associated alterations are deletions, mutations, and methylation of the Ink4a/Arf locus (Kamb et al. 1994; Sherr 1998; Sharpless and DePinho 1999).”
BackgroundThe p16INK4A tumor suppressor regulates cellular oxidative stress
Jenkins, N. C., Liu, T., Cassidy, P., Leachman, S. A., Boucher, K. M., Goodson, A. G., Samadashwily, G., & Grossman, D. (2011) · Oncogene · doi:10.1038/onc.2010.419 · Cited by 138
Bi-allelic Loss of CDKN2A Initiates Melanoma Invasion via BRN2 Activation
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The nucleolus: a central response hub for the stressors that drive cancer progression
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Targeting Cardiac Stem Cell Senescence to Treat Cardiac Aging and Disease
Cianflone, E., Torella, M., Biamonte, F., Angelis, A. D., Urbanek, K., Costanzo, F. S., Rota, M., Ellison, G. M., & Torella, D. (2020) · Cells · doi:10.3390/cells9061558 · Cited by 137
“Bmi-1 targets the repression the INK4a-ARF tumor suppressor gene locus, encoding p16INK4a and p19ARF (called p14ARF in humans), which are key players of the molecular mechanisms of senescence in human and rodent primary cells [85] (Figure 2).”
Backgroundp14ARF silencing by promoter hypermethylation mediates abnormal intracellular localization of MDM2.
Esteller, M., Cordon‐Cardo, C., Corn, P. G., Meltzer, S. J., Pohar, K. S., Watkins, D. N., Capellá, G., Peinado, M. A., Matías‐Guiu, X., Prat, J., et al. (2001) · PubMed · Cited by 132
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“com/oncotarget Complex 1 (PRC1), which overrides cellular senescence and promotes self-renewal [202-204].”
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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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