The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
A comparison of the biological activities of wild‐type and mutant p53
Abstract
Tumorigenesis is characterized by a series of genetic alterations in both dominant oncogenes and tumor suppressor genes. A hallmark of tumor suppressor genes is that both alleles are generally altered during transformation, which usually represents a loss of function phenotype. The p53 tumor suppressor gene is the most frequently affected gene detected in human cancer. There is now growing evidence suggesting that mutation of p53 may involve not only a loss of function of wild‐type p53 activity but also a gain of function phenotype contributed by the mutant p53 protein. The study of the biological properties and functions of both wild‐type and mutant p53 is central to our understanding of human cancer. These properties and functions of wild‐type and mutant p53 will be compared and contrasted here and elsewhere within this thematic issue. In addition, the mechanisms of inactivation of p53 function, which include: 1 ) mutation, 2 ) inhibition by viral oncogene products, 3 ) inhibition by cellular regulators, and 4 ) alteration in subcellular localization, will be discussed.—Zambetti, G. P., Levine, A. J. A comparison of the biological activities of wild‐type and mutant p53. FASEB J. 7: 855‐865; 1993.
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
p53 Mutations in Human Cancers
Hollstein, M., Sidransky, D., Vogelstein, B., & Harris, C. C. (1991) · Science · doi:10.1126/science.1905840 · Cited by 8,018
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
Momand, J., Zambetti, G. P., Olson, D. C., George, D., & Levine, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90644-r · Cited by 3,113
Self-citationKastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047
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
Self-citationDefinition of a consensus binding site for p53
El-Deiry, W. S., Kern, S. E., Pietenpol, J. A., Kinzler, K. W., & Vogelstein, B. (1992) · Nature Genetics · doi:10.1038/ng0492-45 · Cited by 1,985
Amplification of a gene encoding a p53-associated protein in human sarcomas
Oliner, J. D., Kinzler, K. W., Meltzer, P. S., George, D. L., & Vogelstein, B. (1992) · Nature · doi:10.1038/358080a0 · Cited by 1,949
Wild-type p53 activates transcription in vitro
Farmer, G., Bargonetti, J., Zhu, H., Friedman, P., Prywes, R., & Prives, C. (1992) · Nature · doi:10.1038/358083a0 · Cited by 579 · cited 2×
“Purified human and murine wild-type p53 protein can in fact strongly transactivate transcription from a minimal human fos promoter that contains a single 33 bp RGC p53 DNA binding element upstream from the TATA element in an in vitro transcription assay using partially purified HeLa cell nuclear extracts (78).”
BackgroundMethodShaulsky, G., Goldfinger, N., Ben-Ze'ev, A., & Rotter, V (1990) · Molecular and Cellular Biology · doi:10.1128/mcb.10.12.6565 · Cited by 356
The mdm-2 oncogene can overcome wild-type p53 suppression of transformed cell growth.
Finlay, C. A. (1993) · Molecular and Cellular Biology · doi:10.1128/mcb.13.1.301 · Cited by 311
Cited by
Mechanisms Controlling the Function and Life Span of the Corpus Luteum
Niswender, G. D., Juengel, J. L., Silva, P. J., Rollyson, M. K., & McIntush, E. W. (2000) · Physiological Reviews · doi:10.1152/physrev.2000.80.1.1 · Cited by 1,052
Myc pathways provoking cell suicide and cancer
Nilsson, J. A., & Cleveland, J. L. (2003) · Oncogene · doi:10.1038/sj.onc.1207261 · Cited by 462
Barak, Y., Gottlieb, E., Juven-Gershon, T., & Oren, M. (1994) · Genes & Development · doi:10.1101/gad.8.15.1739 · Cited by 328
Mutant p53 Cooperates with ETS and Selectively Up-regulates Human MDR1 Not MRP1
Sampath, J., Sun, D., Kidd, V. J., Grenet, J., Gandhi, A., Shapiro, L. H., Wang, Q., Zambetti, G. P., & Schuetz, J. D. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m103429200 · Cited by 244
Self-citationHui, L., Zheng, Y., Yan, Y., Bargonetti, J., & Foster, D. A. (2006) · Oncogene · doi:10.1038/sj.onc.1209735 · Cited by 218
Metadata
- Authors
- Zambetti, G. P., & Levine, A. J.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 1993-07
- Volume
- 7
- Issue
- 10
- Pages
- 855-865
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W1674633125
- Cited by
- 413
- References
- 10
- FWCI
- 24.08
- Type
- journal article
- Language
- en
- Open access
- closed
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: A comparison of the biological activities of wild‐type and mutant p53. https://app.cochat.ai/papers/10.1096/fasebj.7.10.8344485
- The paper
- Zambetti, G. P., & Levine, A. J. (1993). A comparison of the biological activities of wild‐type and mutant p53. The FASEB Journal. https://doi.org/10.1096/fasebj.7.10.8344485
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.
