Cited by 311Cancer-related Molecular PathwaysCell death mechanisms and regulationHeat shock proteins research

The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.

The mdm-2 oncogene can overcome wild-type p53 suppression of transformed cell growth.

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Finlay, C A·1993·Molecular and Cellular Biology

Abstract

Expression of a p53-associated protein, Mdm-2 (murine double minute-2), can inhibit p53-mediated transactivation. In this study, overexpression of the Mdm-2 protein was found to result in the immortalization of primary rat embryo fibroblasts (REFs) and, in conjunction with an activated ras gene, in the transformation of REFs. The effect of wild-type p53 on the transforming properties of mdm-2 was determined by transfecting REFs with ras, mdm-2, and normal p53 genes. Transfection with ras plus mdm-2 plus wild-type p53 resulted in a 50% reduction in the number of transformed foci (relative to the level for ras plus mdm-2); however, more than half (9 of 17) of the cell lines derived from these foci expressed low levels of a murine p53 protein with the characteristics of a wild-type p53. These results are in contrast to previous studies which demonstrated that even minimal levels of wild-type p53 are not tolerated in cells transformed by ras plus myc, E1A, or mutant p53. The mdm-2 oncogene can overcome the previously demonstrated growth-suppressive properties of p53.

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Crossref · 10.1128/mcb.13.1.301

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Metadata

Authors
Finlay, C. A.
Affiliations
Princeton University (US)
Corresponding author
Finlay, C A
Venue
Molecular and Cellular Biology
Published
1993-01
Volume
13
Issue
1
Pages
301-306
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
OpenAlex
W2137124052
Cited by
311
References
45
Citations by year
2024: 1 · 2023: 1 · 2021: 1 · 2020: 3 · 2019: 4 · 2018: 6 · 2016: 4 · 2015: 6 · 2014: 6 · 2013: 4 · 2012: 6
FWCI
13.87
Type
journal article
Language
en
Open access
Locations
  • Molecular and Cellular Biology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ca055036-03)
  • National Cancer Institute
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
Keywords
MDM2, p53, oncogenes, cell transformation, Ras, cell immortalization, rat embryo fibroblasts, growth inhibition, p53 transactivation, tumor suppressor, transformed foci
MeSH terms
Animals, Cell Division, Cell Transformation, Neoplastic, Neoplasm Proteins, Nuclear Proteins, Precipitin Tests, Proto-Oncogene Proteins, Proto-Oncogenes, Rats, Inbred F344, Oncogene Proteins, Genes, Tumor Suppressor, Tumor Suppressor Protein p53, Rats, Proto-Oncogene Proteins c-mdm2

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