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Cited by 530

The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.

Deregulated expression of E2F-1 induces S-phase entry and leads to apoptosis.

Open access
Shan, B, Lee, W H·1994·Molecular and Cellular Biology

Abstract

E2F-1, the first gene product identified among a family of E2F transcription factors, is thought to play a critical role in G1/S progression of the cell cycle. Transcriptional activities of E2F are modulated during the cell cycle, mainly by the formation of complexes between E2F and several key regulators of cell cycle such as the retinoblastoma protein and related proteins. To further understand the roles of E2F in the cell cycle progression, we have overexpressed exogenous E2F-1 by using a tetracycline-controlled expression system. We have found that the induced expression of E2F-1 in Rat-2 fibroblasts promotes S-phase entry and subsequently leads to apoptosis. The apoptosis occurs in an E2F-1 dose-dependent manner. Cells resistant to the induction of apoptosis have lost the ability to express exogenous E2F-1. Cells growing in low serum are more sensitive to the E2F-1-mediated cell death. Overexpression of E2F-1 mutants that impair DNA binding or transactivation does not alter cell cycle progression or induce apoptosis. These results define a novel pathway to apoptosis and demonstrate that premature S-phase entry is associated with apoptotic cell death.

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Metadata

Authors
Shan, B., & Lee, W. H.
Venue
Molecular and Cellular Biology
Published
1994-12
Volume
14
Issue
12
Pages
8166-8173
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
OpenAlex
W1834050293
Cited by
530
References
57
FWCI
17.72
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Deregulated expression of E2F-1 induces S-phase entry and leads to apoptosis. https://app.cochat.ai/papers/10.1128/mcb.14.12.8166
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Shan, B., & Lee, W. H. (1994). Deregulated expression of E2F-1 induces S-phase entry and leads to apoptosis. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.14.12.8166

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