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Cited by 461

The DOI matches its Crossref record; 100 of the 100 references it cites were found in a registry or an index.

Cell cycle and apoptosis

Open access
Vermeulen, Katrien, Berneman, Zwi N., Van Bockstaele, Dirk R.·2003·Cell Proliferation

Abstract

Abstract. Apoptosis and proliferation are intimately coupled. Some cell cycle regulators can influence both cell division and programmed cell death. The linkage of cell cycle and apoptosis has been recognized for c‐Myc, p53, pRb, Ras, PKA, PKC, Bcl‐2, NF‐κB, CDK, cyclins and CKI. This review summarizes the different functions of the proteins presently known to control both apoptosis and cell cycle progression. These proteins can influence apoptosis or proliferation but different variables, including cell type, cellular environment and genetic background, make it difficult to predict the outcome of cell proliferation, cell cycle arrest or cell death. These important decisions of cell proliferation or cell death are likely to be controlled by more than one signal and are necessary to ensure a proper cellular response.

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Crossref · 10.1046/j.1365-2184.2003.00267.x

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Metadata

Authors
Vermeulen, K., Berneman, Z. N., & Van Bockstaele, D. R.
Venue
Cell Proliferation
Publisher
Wiley
Published
2003-06
Volume
36
Issue
3
Pages
165-175
ISSN
  • 0960-7722 (ISSN-L)
  • 1365-2184
OpenAlex
W2094222260
Cited by
461
References
100
FWCI
10.38
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Cell cycle and apoptosis. https://app.cochat.ai/papers/10.1046/j.1365-2184.2003.00267.x
The paper
Vermeulen, K., Berneman, Z. N., & Van Bockstaele, D. R. (2003). Cell cycle and apoptosis. Cell Proliferation. https://doi.org/10.1046/j.1365-2184.2003.00267.x

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.