The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
20 years studying p53 functions in genetically engineered mice
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Moreover, p53 provides protection against exposure to teratogens during embryogenesis by eliminating damaged embryos and ensuring that only healthy individuals survive (Donehower and Lozano, 2009).”
From p53 at a glance (2010) · cites this paper as Donehower and Lozano, 2009
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 1×
“However, by 1989 the findings that p53 is a tumour suppressor and is frequently mutated in human cancers caused a dramatic upsurge of interest in this gen”
BackgroundMice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Self-citationp53 is required for radiation-induced apoptosis in mouse thymocytes
Lowe, S. W., Schmitt, E. M., Smith, S. W., Osborne, B. A., & Jacks, T. (1993) · Nature · doi:10.1038/362847a0 · Cited by 2,864
Crystal Structure of a p53 Tumor Suppressor-DNA Complex: Understanding Tumorigenic Mutations
Cho, Y., Gorina, S., Jeffrey, P. D., & Pavletich, N. P. (1994) · Science · doi:10.1126/science.8023157 · Cited by 2,551 · cited 1×
“The p53-R172H mutation (corresponding to amino acid 175 in human p53) disrupts the structure of the DNA-binding domain and is one of the most aggressive mutants that has been examined in cell cultur”
BackgroundSenescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
Xue, W., Zender, L., Miething, C., Dickins, R. A., Hernando, E., Krizhanovsky, V., Cordon-Cardo, C., & Lowe, S. W. (2007) · Nature · doi:10.1038/nature05529 · Cited by 2,473
The p53 proto-oncogene can act as a suppressor of transformation
Finlay, C. A., Hinds, P. W., & Levine, A. J. (1989) · Cell · doi:10.1016/0092-8674(89)90045-7 · Cited by 1,987
Restoration of p53 function leads to tumour regression in vivo
Ventura, A., Kirsch, D. G., McLaughlin, M. E., Tuveson, D. A., Grimm, J., Lintault, L., Newman, J., Reczek, E. E., Weissleder, R., & Jacks, T. (2007) · Nature · doi:10.1038/nature05541 · Cited by 1,820 · cited 1×
“The use of such conditionally activated wild-type p53 models was also used by the Evan, Jacks and Lowe laboratories to show that the restoration of p53 function can cause dramatic tumour regressio”
Methodp53 mutant mice that display early ageing-associated phenotypes
Tyner, S. D., Venkatachalam, S., Choi, J., Jones, S., Ghebranious, N., Igelmann, H., Lu, X., Soron, G., Cooper, B., Brayton, C., et al. (2002) · Nature · doi:10.1038/415045a · Cited by 1,459
Self-citationRescue of early embryonic lethality in mdm2-deficient mice by deletion of p53
de Oca Luna, R. M., Wagner, D. S., & Lozano, G. (1995) · Nature · doi:10.1038/378203a0 · Cited by 1,420 · cited 1×
“In 1995 our laboratories showed that aberrant expression of p53 could affect development using Mdm2 -knockout mic”
MethodSelf-citationCloning of senescent cell-derived inhibitors of DNA synthesis using an expression screen
Noda, A., Ning, Y., Venable, S. F., Pereira-Smith, O. M., & Smith, J. R. (1994) · Experimental Cell Research · doi:10.1006/excr.1994.1063 · Cited by 1,351
Research works printed but not linked: 98
- Levine, A. J. p53, the cellular gatekeeper for growth and division. Cell 88, 323–331 (1997). · DOI · Paper page
- Palmiter, R. D. & Brinster, R. L. Germ-line transformation of mice. Annu. Rev. Genet. 20, 465–499 (1986). · DOI · Paper page
- Capecchi, M. R. Altering the genome by homologous recombination. Science 244, 1288–1292 (1989). · DOI · Paper page
- Bradley, A., Ramirez-Solis, R., Zheng, H., Hasty, P. & Davis, A. Genetic manipulation of the mouse via gene targeting in embryonic stem cells. Ciba Found. Symp. 165, 256–69 (1992).
- Lavigueur, A. et al. High incidence of lung, bone, and lymphoid tumors in transgenic mice overexpressing mutant alleles of the p53 oncogene. Mol. Cell. Biol. 9, 3982–3991 (1989). · DOI · Paper page
- Malkin, D. et al. Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms. Science 250, 1233–1238 (1990). · DOI · Paper page
- Srivastava, S., Zou, Z. Q., Pirollo, K., Blattner, W. & Chang, E. H. Germ-line transmission of a mutated p53 gene in a cancer-prone family with Li–Fraumeni syndrome. Nature 348, 747–749 (1990). · DOI · Paper page
- Varley, J. M. Germline TP53 mutations and Li–Fraumeni syndrome. Hum. Mutat. 21, 313–320 (2003). · DOI · Paper page
- Bachinski, L. L. et al. Genetic mapping of a third Li–Fraumeni syndrome predisposition locus to human chromosome 1q23. Cancer Res. 65, 427–431 (2005). · DOI
- Tsukada, T. et al. Enhanced proliferative potential in culture of cells from p53-deficient mice. Oncogene 8, 3313–3322 (1993).
- Jacks, T. et al. Tumor spectrum analysis in p53-mutant mice. Curr. Biol. 4, 1–7 (1994). · DOI · Paper page
- Purdie, C. A. et al. Tumour incidence, spectrum and ploidy in mice with a large deletion in the p53 gene. Oncogene 9, 603–609 (1994).
- Lee, E. Y. et al. Mice deficient for Rb are nonviable and show defects in neurogenesis and haematopoiesis. Nature 359, 288–294 (1992). · DOI · Paper page
- Jacks, T. et al. Effects of an Rb mutation in the mouse. Nature 359, 295–300 (1992). · DOI · Paper page
- Matzuk, M. M., Finegold, M. J., Su, J. G., Hsueh, A. J. & Bradley, A. α-inhibin is a tumour-suppressor gene with gonadal specificity in mice. Nature 360, 313–319 (1992). · DOI · Paper page
- Armstrong, J. F., Kaufman, M. H., Harrison, D. J. & Clarke, A. R. High-frequency developmental abnormalities in p53-deficient mice. Curr. Biol. 5, 931–936 (1995). · DOI · Paper page
- Sah, V. P. et al. A subset of p53-deficient embryos exhibit exencephaly. Nature Genet. 10, 175–180 (1995). · DOI · Paper page
- Marine, J. C. & Lozano, G. Mdm2-mediated ubiquitylation: p53 and beyond. Cell Death Differ. 5 Jun 2009 (doi: 10.1038/cdd.2009.68). · DOI · Paper page
- de Rozieres, S., Maya, R., Oren, M. & Lozano, G. The loss of mdm2 induces p53-mediated apoptosis. Oncogene 19, 1691–1697 (2000). · DOI
- Donehower, L. A. The p53-deficient mouse: a model for basic and applied cancer studies. Semin. Cancer Biol. 7, 269–278 (1996). · DOI · Paper page
- Venkatachalam, S. et al. Is p53 haploinsufficient for tumor suppression? Implications for the p53+/− mouse model in carcinogenicity testing. Toxicol. Pathol. 29, 147–154 (2001). · DOI
- Knudson, A. G. Jr, Hethcote, H. W. & Brown, B. W. Mutation and childhood cancer: a probabilistic model for the incidence of retinoblastoma. Proc. Natl Acad. Sci. USA 72, 5116–5120 (1975). · DOI · Paper page
- Knudson, A. G. Jr. Genetics of human cancer. Annu. Rev. Genet. 20, 231–251 (1986). · DOI · Paper page
- Venkatachalam, S. et al. Retention of wild-type p53 in tumors from p53 heterozygous mice: reduction of p53 dosage can promote cancer formation. EMBO J. 17, 4657–4667 (1998). · DOI · Paper page
- Blackburn, A. C. et al. Loss of heterozygosity occurs via mitotic recombination in Trp53+/− mice and associates with mammary tumor susceptibility of the BALB/c strain. Cancer Res. 64, 5140–5147 (2004). · DOI
- Attardi, L. D. & Donehower, L. A. Probing p53 biological functions through the use of genetically engineered mouse models. Mutat. Res. 576, 4–21 (2005). · DOI
- Lozano, G. The oncogenic roles of p53 mutants in mouse models. Curr. Opin. Genet. Dev. 17, 66–70 (2007). · DOI
- Johnson, T. M. & Attardi, L. D. Dissecting p53 tumor suppressor function in vivo through the analysis of genetically modified mice. Cell Death Differ. 13, 902–908 (2006). · DOI
- Clarke, A. R. et al. Thymocyte apoptosis induced by p53-dependent and independent pathways. Nature 362, 849–852 (1993). · DOI · Paper page
- Sigal, A. & Rotter, V. Oncogenic mutations of the p53 tumor suppressor: the demons of the guardian of the genome. Cancer Res. 60, 6788–6793 (2000).
- Dittmer, D. et al. Gain of function mutations in p53. Nature Genet. 4, 42–46 (1993). · DOI · Paper page
- Liu, G. et al. High metastatic potential in mice inheriting a targeted p53 missense mutation. Proc. Natl Acad. Sci. USA 97, 4174–4179 (2000). · DOI · Paper page
- Lang, G. A. et al. Gain of function of a p53 hot spot mutation in a mouse model of Li–Fraumeni syndrome. Cell 119, 861–872 (2004). · DOI · Paper page
- Terzian, T. et al. The inherent instability of mutant p53 is alleviated by Mdm2 or p16INK4a loss. Genes Dev. 22, 1337–1344 (2008). · DOI · Paper page
- Ljungman, M. Dial 9-1-1 for p53: mechanisms of p53 activation by cellular stress. Neoplasia 2, 208–225 (2000). · DOI
- Eischen, C. M. & Lozano, G. p53 and MDM2: antagonists or partners in crime? Cancer Cell 15, 161–162 (2009). · DOI
- McDonnell, T. J. et al. Loss of one but not two mdm2 null alleles alters the tumour spectrum in p53 null mice. J. Pathol. 188, 322–328 (1999). · DOI · Paper page
- Flores, E. R. et al. Tumor predisposition in mice mutant for p63 and p73: evidence for broader tumor suppressor functions for the p53 family. Cancer Cell 7, 363–373 (2005). · DOI · Paper page
- el-Deiry, W. S. et al. WAF1, a potential mediator of p53 tumor suppression. Cell 75, 817–825 (1993). · DOI · Paper page
- Barboza, J. A., Liu, G., Ju, Z., El-Naggar, A. K. & Lozano, G. p21 delays tumor onset by preservation of chromosomal stability. Proc. Natl Acad. Sci. USA 103, 19842–19847 (2006). · DOI
- Iwakuma, T. & Lozano, G. Crippling p53 activities via knock-in mutations in mouse models. Oncogene 26, 2177–2184 (2007). · DOI
- Armata, H. L., Garlick, D. S. & Sluss, H. K. The ataxia telangiectasia-mutated target site Ser18 is required for p53-mediated tumor suppression. Cancer Res. 67, 11696–11703 (2007). · DOI
- Chao, C., Herr, D., Chun, J. & Xu, Y. Ser18 and 23 phosphorylation is required for p53-dependent apoptosis and tumor suppression. EMBO J. 25, 2615–2622 (2006).
- Marino, S., Vooijs, M., van Der Gulden, H., Jonkers, J. & Berns, A. Induction of medulloblastomas in p53-null mutant mice by somatic inactivation of Rb in the external granular layer cells of the cerebellum. Genes Dev. 14, 994–1004 (2000). · DOI · Paper page
- Berman, S. D. et al. Metastatic osteosarcoma induced by inactivation of Rb and p53 in the osteoblast lineage. Proc. Natl Acad. Sci. USA 105, 11851–11856 (2008). · DOI · Paper page
- Lengner, C. J. et al. Osteoblast differentiation and skeletal development are regulated by Mdm2–p53 signaling. J. Cell. Biol. 172, 909–921 (2006). · DOI · Paper page
- Lin, S. C. et al. Somatic mutation of p53 leads to estrogen receptor α-positive and -negative mouse mammary tumors with high frequency of metastasis. Cancer Res. 64, 3525–3532 (2004). · DOI
- Walkley, C. R. et al. Conditional mouse osteosarcoma, dependent on p53 loss and potentiated by loss of Rb, mimics the human disease. Genes Dev. 22, 1662–1676 (2008). · DOI · Paper page
- Hinkal, G. W., Parikh, N. & Donehower, L. A. Timed somatic deletion of p53 in mice reveals age-associated differences in tumor progression. PLoS ONE 4, e6654 (2009). · DOI
- Seibler, J. et al. Rapid generation of inducible mouse mutants. Nucleic Acids Res. 31, e12 (2003). · DOI · Paper page
- Wijnhoven, S. W. et al. Mice expressing a mammary gland-specific R270H mutation in the p53 tumor suppressor gene mimic human breast cancer development. Cancer Res. 65, 8166–8173 (2005). · DOI
- Christophorou, M. A. et al. Temporal dissection of p53 function in vitro and in vivo. Nature Genet. 37, 718–726 (2005). · DOI · Paper page
- Ringshausen, I., O'Shea, C. C., Finch, A. J., Swigart, L. B. & Evan, G. I. Mdm2 is critically and continuously required to suppress lethal p53 activity in vivo. Cancer Cell 10, 501–514 (2006). · DOI · Paper page
- Nicol, C. J., Harrison, M. L., Laposa, R. R., Gimelshtein, I. L. & Wells, P. G. A teratologic suppressor role for p53 in benzo(a)pyrene-treated transgenic p53-deficient mice. Nature Genet. 10, 181–187 (1995). · DOI · Paper page
- Norimura, T., Nomoto, S., Katsuki, M., Gondo, Y. & Kondo, S. p53-dependent apoptosis suppresses radiation-induced teratogenesis. Nature Med. 2, 577–580 (1996). · DOI
- Wang, B. Involvement of p53-dependent apoptosis in radiation teratogenesis and in the radioadaptive response in the late organogenesis of mice. J. Radiat. Res. 42, 1–10 (2001). · DOI
- Finch, R. A. et al. mdmx is a negative regulator of p53 activity in vivo. Cancer Res. 62, 3221–3225 (2002).
- Hu, W., Feng, Z., Teresky, A. K. & Levine, A. J. p53 regulates maternal reproduction through LIF. Nature 450, 721–724 (2007). · DOI · Paper page
- Kay, C., Jeyendran, R. S. & Coulam, C. B. p53 tumour suppressor gene polymorphism is associated with recurrent implantation failure. Reprod. Biomed. Online 13, 492–496 (2006). · DOI
- Hu, W., Feng, Z., Atwal, G. S. & Levine, A. J. p53: a new player in reproduction. Cell Cycle 7, 848–852 (2008). · DOI
- de Vries, A. et al. Targeted point mutations of p53 lead to dominant-negative inhibition of wild-type p53 function. Proc. Natl Acad. Sci. USA 99, 2948–2953 (2002). · DOI · Paper page
- Maier, B. et al. Modulation of mammalian life span by the short isoform of p53. Genes Dev. 18, 306–319 (2004). · DOI · Paper page
- Garcia-Cao, I. et al. “Super p53” mice exhibit enhanced DNA damage response, are tumor resistant and age normally. EMBO J. 21, 6225–6235 (2002).
- Ferbeyre, G. & Lowe, S. W. The price of tumour suppression? Nature 415, 26–27 (2002). · DOI
- Dumble, M. et al. The impact of altered p53 dosage on hematopoietic stem cell dynamics during aging. Blood 109, 1736–1742 (2007). · DOI · Paper page
- Akala, O. O. et al. Long-term haematopoietic reconstitution by Trp53−/−p16 Ink4A−/−p19 Arf−/− multipotent progenitors. Nature 453, 228–232 (2008). · DOI · Paper page
- Gatza, C., Moore, L., Dumble, M. & Donehower, L. A. Tumor suppressor dosage regulates stem cell dynamics during aging. Cell Cycle 6, 52–55 (2007). · DOI
- Bourdon, J. C. p53 Family isoforms. Curr. Pharm. Biotechnol. 8, 332–336 (2007). · DOI
- Mills, A. A. p63: oncogene or tumor suppressor? Curr. Opin. Genet. Dev. 16, 38–44 (2006). · DOI
- Rosenbluth, J. M. & Pietenpol, J. A. The jury is in: p73 is a tumor suppressor after all. Genes Dev. 22, 2591–2595 (2008). · DOI
- Mills, A. A. et al. p63 is a p53 homologue required for limb and epidermal morphogenesis. Nature 398, 708–713 (1999). · DOI · Paper page
- Yang, A. et al. p63 is essential for regenerative proliferation in limb, craniofacial and epithelial development. Nature 398, 714–718 (1999). · DOI · Paper page
- Keyes, W. M. et al. p63 deficiency activates a program of cellular senescence and leads to accelerated aging. Genes Dev. 19, 1986–1999 (2005). · DOI · Paper page
- Keyes, W. M. et al. p63 heterozygous mutant mice are not prone to spontaneous or chemically induced tumors. Proc. Natl Acad. Sci. USA 103, 8435–8440 (2006). · DOI
- Yang, A. et al. p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours. Nature 404, 99–103 (2000). · DOI · Paper page
- Tomasini, R. et al. TAp73 knockout shows genomic instability with infertility and tumor suppressor functions. Genes Dev. 22, 2677–2691 (2008). · DOI · Paper page
- Tomasini, R., Mak, T. W. & Melino, G. The impact of p53 and p73 on aneuploidy and cancer. Trends Cell Biol. 18, 244–252 (2008). · DOI
- Kuperwasser, C. et al. Development of spontaneous mammary tumors in BALB/c p53 heterozygous mice. A model for Li—Fraumeni syndrome. Am. J. Pathol. 157, 2151–2159 (2000). · DOI · Paper page
- Harvey, M., McArthur, M. J., Montgomery, C. A. Jr, Bradley, A. & Donehower, L. A. Genetic background alters the spectrum of tumors that develop in p53- deficient mice. FASEB J. 7, 938–943 (1993). · DOI · Paper page
- Johnson, T. M., Hammond, E. M., Giaccia, A. & Attardi, L. D. The p53QS transactivation-deficient mutant shows stress-specific apoptotic activity and induces embryonic lethality. Nature Genet. 37, 145–152 (2005). · DOI
- Nister, M. et al. p53 must be competent for transcriptional regulation to suppress tumor formation. Oncogene 24, 3563–3573 (2005). · DOI
- Chao, C. et al. Acetylation of mouse p53 at lysine 317 negatively regulates p53 apoptotic activities after DNA damage. Mol. Cell. Biol. 26, 6859–6869 (2006). · DOI
- Krummel, K. A., Lee, C. J., Toledo, F. & Wahl, G. M. The C-terminal lysines fine-tune p53 stress responses in a mouse model but are not required for stability control or transactivation. Proc. Natl Acad. Sci. USA 102, 10188–10193 (2005). · DOI · Paper page
- Luo, J. L. et al. Knock-in mice with a chimeric human/murine p53 gene develop normally and show wild-type p53 responses to DNA damaging agents: a new biomedical research tool. Oncogene 20, 320–328 (2001). · DOI
- Song, H., Hollstein, M. & Xu, Y. p53 gain-of-function cancer mutants induce genetic instability by inactivating ATM. Nature Cell Biol. 9, 573–580 (2007). · DOI · Paper page
- Johnson, T. M., Meade, K., Pathak, N., Marques, M. R. & Attardi, L. D. Knockin mice expressing a chimeric p53 protein reveal mechanistic differences in how p53 triggers apoptosis and senescence. Proc. Natl Acad. Sci. USA 105, 1215–1220 (2008). · DOI
- Jonkers, J. et al. Synergistic tumor suppressor activity of BRCA2 and p53 in a conditional mouse model for breast cancer. Nature Genet. 29, 418–425 (2001). · DOI · Paper page
- Ghebranious, N. & Sell, S. The mouse equivalent of the human p53ser249 mutation p53ser246 enhances aflatoxin hepatocarcinogenesis in hepatitis B surface antigen transgenic and p53 heterozygous null mice. Hepatology 27, 967–973 (1998). · DOI
- Li, B., Rosen, J. M., McMenamin-Balano, J., Muller, W. J. & Perkins, A. S. neu/ERBB2 cooperates with p53–172H during mammary tumorigenesis in transgenic mice. Mol. Cell. Biol. 17, 3155–3163 (1997). · DOI
- Li, B. et al. Preferential overexpression of a 172Arg-->Leu mutant p53 in the mammary gland of transgenic mice results in altered lobuloalveolar development. Cell Growth Differ. 5, 711–721 (1994).
- Hernandez, I. et al. Prostate-specific expression of p53R172L differentially regulates p21, Bax, and mdm2 to inhibit prostate cancer progression and prolong survival. Mol. Cancer Res. 1, 1036–1047 (2003).
- Duan, W. et al. Lung-specific expression of human mutant p53–273H is associated with a high frequency of lung adenocarcinoma in transgenic mice. Oncogene 21, 7831–7838 (2002). · DOI
- Klein, M. A. et al. Reduced latency but no increased brain tumor penetrance in mice with astrocyte specific expression of a human p53 mutant. Oncogene 19, 5329–5337 (2000). · DOI
- Godley, L. A. et al. Wild-type p53 transgenic mice exhibit altered differentiation of the ureteric bud and possess small kidneys. Genes Dev. 10, 836–850 (1996). · DOI
- Gillet, R. et al. The consequence of p53 overexpression for liver tumor development and the response of transformed murine hepatocytes to genotoxic agents. Oncogene 19, 3498–3507 (2000). · DOI
- Kemp, C. J., Donehower, L. A., Bradley, A. & Balmain, A. Reduction of p53 gene dosage does not increase initiation or promotion but enhances malignant progression of chemically induced skin tumors. Cell 74, 813–822 (1993). · DOI · Paper page
- Howes, K. A. et al. Apoptosis or retinoblastoma: alternative fates of photoreceptors expressing the HPV-16 E7 gene in the presence or absence of p53. Genes Dev. 8, 1300–1310 (1994). · DOI · Paper page
- Schmitt, C. A. et al. A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy. Cell 109, 335–346 (2002). · DOI · Paper page
Cited by
The first 30 years of p53: growing ever more complex.
Levine, A. J., & Oren, M. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2723 · Cited by 1,967
Linking functional decline of telomeres, mitochondria and stem cells during ageing
Sahin, E., & DePinho, R. A. (2010) · Nature · doi:10.1038/nature08982 · Cited by 759
The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer Therapeutics
Hata, A. N., Engelman, J. A., & Faber, A. C. (2015) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-0011 · Cited by 619
Brady, C. A., & Attardi, L. D. (2010) · Journal of Cell Science · doi:10.1242/jcs.064501 · Cited by 403
Soussi, T., & Wiman, K. G. (2015) · Cell Death & Differentiation · doi:10.1038/cdd.2015.53 · Cited by 305
Metadata
- Authors
- Donehower, L. A., & Lozano, G.
- Venue
- Nature Reviews Cancer
- Published
- 2009-09-24
- Volume
- 9
- Issue
- 11
- Pages
- 831-841
- ISSN
- 1474-175X
- 1474-1768
- Cited by
- 168
- References
- 37
- Language
- en
- Licence
- www.springer.com/tdm (tdm)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: 20 years studying p53 functions in genetically engineered mice. https://app.cochat.ai/papers/10.1038/nrc2731
- The paper
- Donehower, L. A., & Lozano, G. (2009). 20 years studying p53 functions in genetically engineered mice. Nature Reviews Cancer. https://doi.org/10.1038/nrc2731
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.