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Cyclin G is a transcriptional target of the p53 tumor suppressor protein.
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Through a PCR-based differential screening method, cyclin G was identified as a novel transcriptional target of the p53 tumor suppressor gene product. In both a mouse p53 temperature-sensitive leukemic cell line and mouse embryonic fibroblasts (MEF) after gamma-irradiation, cyclin G mRNA was rapidly induced. MEF from a p53-deficient mouse expressed cyclin G at a level > 10-fold lower than that from a wild-type mouse. Using a DNA binding assay, a specific p53 binding site was identified upstream from the cyclin G gene, which functioned as a p53-dependent cis-acting element in a transient transfection assay. These results suggest that cyclin G might participate in a p53-mediated pathway to prevent tumorigenesis.
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“MDM2 function is supported through cyclin G1, which activates MDM2 through dephosphorylation218 and CCNG1 is a p53 target itself.219”
From Census and evaluation of p53 target genes (2017) · cites this paper as [219]
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Yamauchi, Y., Tanaka, A., Yamaguchi, K., Kobayashi, M., Shimamura, S., & Hanaoka, F. (1998) · Experimental Cell Research · doi:10.1006/excr.1997.3841 · Cited by 3
Metadata
- Authors
- Okamoto, K., & Beach, D.
- Affiliations
- Howard Hughes Medical Institute (US)
- ORCID
- Okamoto, K.
- Venue
- The EMBO Journal
- Published
- 1994-10-01
- Volume
- 13
- Issue
- 20
- Pages
- 4816-4822
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC395420
- OpenAlex
- W1823168351
- Cited by
- 455
- References
- 40
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 1 · 2023: 7 · 2022: 2 · 2021: 3 · 2020: 5 · 2019: 5 · 2018: 5 · 2017: 7 · 2016: 3 · 2015: 11 · 2014: 6 · 2013: 10 · 2012: 11
- FWCI
- 15.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health
- National Institute of General Medical Sciences (GM 396 20-06)
- 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
- cyclin G, p53, transcription factor target genes, tumor suppressor, p53 binding sites, cis-regulatory elements, gamma irradiation, carcinogenesis, mouse embryonic fibroblasts, leukemia cell lines
- MeSH terms
- Amino Acid Sequence, Animals, Base Sequence, Cells, Cultured, Molecular Sequence Data, Protein Binding, Transcription Factors, Tumor Cells, Cultured, Transcriptional Activation, Tumor Suppressor Protein p53, Cyclins, Mice, Cyclin G, Cyclin G1
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.
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