The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
TAp73 knockout shows genomic instability with infertility and tumor suppressor functions
Open accessAbstract
The Trp53 gene family member Trp73 encodes two major groups of protein isoforms, TAp73 and ΔNp73, with opposing pro- and anti-apoptotic functions; consequently, their relative ratio regulates cell fate. However, the precise roles of p73 isoforms in cellular events such as tumor initiation, embryonic development, and cell death remain unclear. To determine which aspects of p73 function are attributable to the TAp73 isoforms, we generated and characterized mice in which exons encoding the TAp73 isoforms were specifically deleted to create a TAp73-deficient (TAp73 −/− ) mouse. Here we show that mice specifically lacking in TAp73 isoforms develop a phenotype intermediate between the phenotypes of Trp73 −/− and Trp53 −/− mice with respect to incidence of spontaneous and carcinogen-induced tumors, infertility, and aging, as well as hippocampal dysgenesis. In addition, cells from TAp73 −/− mice exhibit genomic instability associated with enhanced aneuploidy, which may account for the increased incidence of spontaneous tumors observed in these mutants. Hence, TAp73 isoforms exert tumor-suppressive functions and indicate an emerging role for Trp73 in the maintenance of genomic stability.
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.
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
Mice 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
p53 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 · cited 1×
“The p53-family members are pivotal in the control of aging, as shown for p63 (Keyes et al. 2005; Suh et al. 2006), p53 mutant (Tyner et al. 2002), or deficient mice (Ohkusu-Tsukada et al. 1999).”
Backgroundp53 isoforms can regulate p53 transcriptional activity
Bourdon, J.-C., Fernandes, K., Murray-Zmijewski, F., Liu, G., Diot, A., Xirodimas, D. P., Saville, M. K., & Lane, D. P. (2005) · Genes & Development · doi:10.1101/gad.1339905 · Cited by 810
The p53 family in differentiation and tumorigenesis
Stiewe, T. (2007) · Nature Reviews Cancer · doi:10.1038/nrc2072 · Cited by 306
Cited by
Galluzzi, L., Vitale, I., Abrams, J. M., Alnemri, E. S., Baehrecke, E. H., Blagosklonny, M. V., Dawson, T. M., Dawson, V. L., El-Deiry, W. S., Fulda, S., et al. (2012) · Cell Death & Differentiation · doi:10.1038/cdd.2011.96 · Cited by 2,421
Self-citationThe 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
Muller, P. A. J., & Vousden, K. H. (2013) · Nature Cell Biology · doi:10.1038/ncb2641 · Cited by 1,647
Senescence and aging: the critical roles of p53
Rufini, A., Tucci, P., Celardo, I., & Melino, G. (2013) · Oncogene · doi:10.1038/onc.2012.640 · Cited by 798
Self-citationp63 and p73, the ancestors of p53
Dotsch, V., Bernassola, F., Coutandin, D., Candi, E., & Melino, G. (2010) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a004887 · Cited by 326
Self-citation
Metadata
- Authors
- Tomasini, R., Tsuchihara, K., Wilhelm, M., Fujitani, M., Rufini, A., Cheung, C. C., Khan, F., Itie-Youten, A., Wakeham, A., Tsao, M.-S., Iovanna, J. L., Squire, J., Jurisica, I., Kaplan, D., Melino, G., Jurisicova, A., & Mak, T. W.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2008-09-19
- Volume
- 22
- Issue
- 19
- Pages
- 2677-2691
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2100610935
- Cited by
- 429
- References
- 4
- Type
- posted content
- Language
- en
- Open access
- diamond
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: TAp73 knockout shows genomic instability with infertility and tumor suppressor functions. https://app.cochat.ai/papers/10.1101/gad.1695308
- The paper
- Tomasini, R., Tsuchihara, K., Wilhelm, M., Fujitani, M., Rufini, A., Cheung, C. C., Khan, F., Itie-Youten, A., Wakeham, A., Tsao, M.-S., Iovanna, J. L., Squire, J., Jurisica, I., Kaplan, D., Melino, G., Jurisicova, A., & Mak, T. W. (2008). TAp73 knockout shows genomic instability with infertility and tumor suppressor functions. Genes & Development. https://doi.org/10.1101/gad.1695308
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.
