The DOI matches its Crossref record; 65 of the 70 references it cites were found in a registry or an index.
Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
Open accessAbstract
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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“p21 is required for p53-mediated G1/S146, 147, 148 and also for G2/M cell cycle arrest.149”
From Census and evaluation of p53 target genes (2017) · cites this paper as [148]
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Cites
WAF1, a potential mediator of p53 tumor suppression
El-Deiry, W. S., Tokino, T., Velculescu, V. E., Levy, D. B., Parsons, R., Trent, J. M., Lin, D., Mercer, W. E., Kinzler, K. W., & Vogelstein, B. (1993) · Cell · doi:10.1016/0092-8674(93)90500-p · Cited by 8,321
p53 Mutations in Human Cancers
Hollstein, M., Sidransky, D., Vogelstein, B., & Harris, C. C. (1991) · Science · doi:10.1126/science.1905840 · Cited by 8,018
The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases.
Wade Harper, J. (1993) · Cell · doi:10.1016/0092-8674(93)90499-g · Cited by 5,651
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
Toshiyuki, M., & Reed, J. C. (1995) · Cell · doi:10.1016/0092-8674(95)90412-3 · Cited by 4,063
Participation of p53 protein in the cellular response to DNA damage.
Kastan, M. B., Onyekwere, O. C., Sidransky, D., Vogelstein, B., & Craig, R. W. (1991) · PubMed · Cited by 3,761
p21 is a universal inhibitor of cyclin kinases
Xiong, Y., Hannon, G., Zhang, H., Casso, D., Kobayashi, R., & Beach, D. (1993) · Nature · doi:10.1038/366701a0 · Cited by 3,691
Inhibitors of mammalian G1 cyclin-dependent kinases.Preprint
Sherr, C. J., & Roberts, J. M. (1995) · Genes & Development · doi:10.1101/gad.9.10.1149 · Cited by 3,242
Kastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047
p53 is required for radiation-induced apoptosis in mouse thymocytes
Lowe, S. W., Schmitt, E. M., Smith, S. W., Osborne, B. A., & Jacks, T. (1993) · Nature · doi:10.1038/362847a0 · Cited by 2,864
Research works printed but not linked: 3
- Jiang, 1994, Induction of differentiation in human promyelocytic HL60 leukemia cells activates p21WAF1/CIP1 expression in the absence of p53, Oncogene, 9, 3397
- Steinman, 1994, Induction of p21 (WAFf1CIPl) during differentiation, Oncogene, 9, 3389
- Strasser, 1993, Eubcl2 transgene facilitates spontaneaous transformation of early pre-B and Ig secreting cells but not T cells, Oncogene, 8, 1
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Items 1,001–1,008 of 1,008
p21 limits S phase DNA damage caused by the Wee1 inhibitor MK1775
Hauge, S., Macurek, L., & Syljuåsen, R. G. (2019) · Cell Cycle · doi:10.1080/15384101.2019.1593649 · Cited by 30
Ionizing radiation induces ATM-independent degradation of p21Cip1 in transformed cells
Stuart, S. A., & Wang, J. Y. J. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m808810200 · Cited by 28
p21 WAF1 /Cip1 limits senescence and acinar‐to‐ductal metaplasia formation during pancreatitis
Grabliauskaite, K., Hehl, A. B., Seleznik, G. M., Saponara, E., Schlesinger, K., Zuellig, R. A., Dittmann, A., Bain, M., Reding, T., Sonda, S., et al. (2015) · The Journal of Pathology · doi:10.1002/path.4440 · Cited by 27
Distinct p21 requirements for regulating normal and self-reactive T cells through IFN-γ production
Daszkiewicz, L., Vázquez-Mateo, C., Rackov, G., Ballesteros-Tato, A., Weber, K., Madrigal-Avilés, A., Di Pilato, M., Fotedar, A., Fotedar, R., Flores, J. M., et al. (2015) · Scientific Reports · doi:10.1038/srep07691 · Cited by 26
Hdm2- and proteasome-dependent turnover limits p21 accumulation during S phase
Ciznadija, D., Zhu, X.-H., & Koff, A. (2011) · Cell Cycle · doi:10.4161/cc.10.16.16725 · Cited by 11
Wilson (1999) · doi:10.1002/1529-0131(199907)42:7
Metadata
- Authors
- Deng, C., Zhang, P., Wade Harper, J., Elledge, S. J., & Leder, P.
- Affiliations
- Baylor College of Medicine (US)
- Howard Hughes Medical Institute (US)
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1995-08
- Volume
- 82
- Issue
- 4
- Pages
- 675-684
- ISSN
- 0092-8674 (ISSN-L)
- 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
- 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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