The DOI matches its Crossref record; 64 of the 64 references it cites were found in a registry or an index.
Cellular Transformation and Malignancy Induced by ras Require c-jun
Open accessAbstract
ras is an important oncogene in experimental animals and humans. In addition, activated ras proteins are potent inducers of the transcription factor AP-1, which is composed of heterodimeric complexes of Fos and Jun proteins. Together with the fact that deregulated expression of some AP-1 proteins can cause neoplastic transformation, this finding suggests that AP-1 may function as a critical ras effector. We have tested this hypothesis directly by analyzing the response to activated ras in cells that harbor a null mutation in the c-jun gene. The transcriptional response of AP-1-responsive genes to activated ras is severely impaired in c-jun null fibroblasts. Compared with wild-type cells, the c-jun null cells lack many characteristics of ras transformation, including loss of contact inhibition, anchorage independence, and tumorigenicity in nude mice; these properties are restored by forced expression of c-jun. Rare tumorigenic variants of ras-expressing c-jun null fibroblasts do arise. Analysis of these variants reveals a consistent restoration of AP-1 activity. The results provide genetic evidence that c-jun is a crucial effector for transformation by activated ras proteins.
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Metadata
- Authors
- Johnson, R., Spiegelman, B., Hanahan, D., & Wisdom, R.
- Affiliations
- University of California, San Francisco (US)
- Harvard University (US)
- Vanderbilt University (US)
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 1996-08
- Volume
- 16
- Issue
- 8
- Pages
- 4504-4511
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC231449
- OpenAlex
- W1895834181
- Cited by
- 282
- References
- 61
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 5 · 2022: 1 · 2021: 4 · 2020: 6 · 2019: 2 · 2018: 3 · 2017: 1 · 2016: 6 · 2015: 7 · 2014: 4 · 2013: 8 · 2012: 2
- FWCI
- 6.82
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Molecular and Cellular Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Cancer Society
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- c-Jun, oncogenic Ras, AP-1 transcription factor, Fos-Jun heterodimer, oncogenic transformation, anchorage-independent growth, tumorigenicity, Ras effectors
- MeSH terms
- Animals, Base Sequence, Cell Cycle, Cell Transformation, Neoplastic, Cells, Cultured, Molecular Sequence Data, Oligodeoxyribonucleotides, Genes, ras, Proto-Oncogene Proteins p21(ras), Proto-Oncogene Proteins c-jun, Genes, jun, Mice, Knockout, Mice
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