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Cyclin G is a transcriptional target of the p53 tumor suppressor protein.
Open accessAbstract
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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Götz, C., Scholtes, P., Prowald, A., Schuster, N., Nastainczyk, W., & Montenarh, M. (1999) · Molecular and Cellular Biochemistry · doi:10.1023/a:1006886727248 · Cited by 27
Integration of the PRB and P53 Cell Cycle Control Pathways
Stewart, C. L., Soria, A. M., & Hamel, P. A. (2001) · Journal of Neuro-Oncology · doi:10.1023/a:1010615822317 · Cited by 27
Repression of Human Reduced Folate Carrier Gene Expression by Wild Type p53
Ding, B. C., Whetstine, J. R., Witt, T. L., Schuetz, J. D., & Matherly, L. H. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m005248200 · Cited by 26
Evidence for the interaction of the regulatory protein Ki-1/57 with p53 and its interacting proteins
Nery, F. C., Rui, E., Kuniyoshi, T. M., & Kobarg, J. (2006) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2006.01.036 · Cited by 26
p53 suppresses cytokine induced, Stat5 mediated activation of transcription
Fritsche, M., Mundt, M., Merkle, C., Jähne, R., & Groner, B. (1998) · Molecular and Cellular Endocrinology · doi:10.1016/s0303-7207(98)00140-3 · Cited by 26
Targeting gene expression to tumor cells with loss of wild-type p53 function
Zhu, J., Gao, B., Zhao, J., & Balmain, A. (2000) · Cancer Gene Therapy · doi:10.1038/sj.cgt.7700091 · Cited by 26
Overexpression of DRAM enhances p53‐dependent apoptosis
Takahashi, M., Kakudo, Y., Takahashi, S. I., Sakamoto, Y., Kato, S., & Ishioka, C. (2012) · Cancer Medicine · doi:10.1002/cam4.39 · Cited by 25
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
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