The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
A role for transcriptional repression of p21 CIP1 by c-Myc in overcoming transforming growth factor β-induced cell-cycle arrest
Open accessAbstract
c-Myc plays a vital role in cell-cycle progression. Deregulated expression of c-Myc can overcome cell-cycle arrest in order to promote cellular proliferation. Transforming growth factor β (TGFβ) treatment of immortalized human keratinocyte cells inhibits cell-cycle progression and is characterized by down-regulation of c-Myc followed by up-regulation of p21 CIP1 . A direct role of c-Myc in this pathway was demonstrated by the observation that ectopic expression of c-Myc overcame the cell-cycle block induced by TGFβ treatment. The induction of p21 CIP1 transcription by TGFβ was blocked in human keratinocyte cells stably expressing c-Myc. Furthermore, overexpression of c-Myc in NIH 3T3 cells repressed the basal levels of p21 CIP1 mRNA. Repression of p21 CIP1 transcription by c-Myc occurred at the promoter level in a region near the start site of transcriptional initiation and was independent of histone deacetylase activity. These data suggest that the down-regulation of c-Myc after TGFβ signaling is important for subsequent regulation of p21 CIP1 and cell-cycle inhibition. Thus, repression of the cell-cycle inhibitory gene p21 CIP1 plays a role in c-Myc-dependent cell-cycle progression.
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Cited by
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Metadata
- Authors
- Claassen, G. F., & Hann, S. R.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2000-08
- Volume
- 97
- Issue
- 17
- Pages
- 9498-9503
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2091851050
- Cited by
- 256
- References
- 61
- FWCI
- 6.76
- Type
- journal article
- Language
- en
- Open access
- green
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- Claassen, G. F., & Hann, S. R. (2000). A role for transcriptional repression of p21 CIP1 by c-Myc in overcoming transforming growth factor β-induced cell-cycle arrest. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.150006697
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