Cited by 2,113Cancer-related Molecular PathwaysDNA Repair MechanismsCell death mechanisms and regulation

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Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control

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Deng, Chuxia, Zhang, Pumin, Wade Harper, J., Elledge, Stephen J., Leder, Philip·1995·Cell

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Abstract

p21CIP1/WAF1 is a CDK inhibitor regulated by the tumor suppressor p53 and is hypothesized to mediate G1 arrest. p53 has been suggested to derive anti-oncogenic properties from this relationship. To test these notions, we created mice lacking p21CIP1/WAF1. They develop normally and (unlike p53-/- mice) have not developed spontaneous malignancies during 7 months of observation. Nonetheless, p21-/- embryonic fibroblasts are significantly deficient in their ability to arrest in G1 in response to DNA damage and nucleotide pool perturbation. p21-/- cells also exhibit a significant growth alteration in vitro, achieving a saturation density as high as that observed in p53-/- cells. In contrast, other aspects of p53 function, such as thymocytic apoptosis and the mitotic spindle checkpoint, appear normal. These results establish the role of p21CIP1/WAF1 in the G1 checkpoint, but suggest that the anti-apoptotic and the anti-oncogenic effects of p53 are more complex.

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Authors: Deng, C., Zhang, P., Wade Harper, J., Elledge, S. J., & Leder, P.
Affiliations: Baylor College of Medicine (US)
Howard Hughes Medical Institute (US)
ORCID: Zhang, Pumin
Elledge, Stephen J.
Venue: Cell
Publisher: Elsevier BV
Published: 1995-08
Volume: 82
Issue: 4
Pages: 675-684
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/0092-8674(95)90039-x
OpenAlex: W2044057392
Cited by: 2,113
References: 70
Citations by year: 2026: 20 · 2025: 20 · 2024: 32 · 2023: 32 · 2022: 34 · 2021: 40 · 2020: 38 · 2019: 40 · 2018: 43 · 2017: 36 · 2016: 37 · 2015: 34 · 2014: 57 · 2013: 39 · 2012: 65
FWCI: 61.04
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 6560 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Funders: Howard Hughes Medical Institute
National Institutes of Health
National Institute on Aging (AG11085, R01AG011085)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords: p21, p53, G1/S checkpoint, cyclin-dependent kinase inhibitors, DNA damage response, embryonic fibroblasts, cell growth, thymocyte apoptosis, mitotic spindle checkpoint, tumor suppression
MeSH terms: Animals, Base Sequence, Cell Differentiation, Cell Division, Cell Line, DNA, DNA Damage, Spindle Apparatus, Molecular Sequence Data, Neoplasms, Experimental, Genes, p53, Tumor Suppressor Protein p53, G1 Phase, Cyclins, Apoptosis, Cyclin-Dependent Kinase Inhibitor p21, Mice

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Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control

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