Cited by 3,047Cancer-related Molecular PathwaysDNA Repair MechanismsEffects of Radiation Exposure

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A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

Kastan, Michael B., Zhan, Qimin, El-Deiry, Wafik S., Carrier, France, Jacks, Tyler, Walsh, William V., Plunkett, Beverly S., Vogelstein, Bert, Fornace, Albert J.·1992·Cell

DOI 10.1016/0092-8674(92)90593-2

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Abstract

Cell cycle checkpoints can enhance cell survival and limit mutagenic events following DNA damage. Primary murine fibroblasts became deficient in a G1 checkpoint activated by ionizing radiation (IR) when both wild-type p53 alleles were disrupted. In addition, cells from patients with the radiosensitive, cancer-prone disease ataxia-telangiectasia (AT) lacked the IR-induced increase in p53 protein levels seen in normal cells. Finally, IR induction of the human GADD45 gene, an induction that is also defective in AT cells, was dependent on wild-type p53 function. Wild-type but not mutant p53 bound strongly to a conserved element in the GADD45 gene, and a p53-containing nuclear factor, which bound this element, was detected in extracts from irradiated cells. Thus, we identified three participants (AT gene(s), p53, and GADD45) in a signal transduction pathway that controls cell cycle arrest following DNA damage; abnormalities in this pathway probably contribute to tumor development.

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Self-citation

Authors: Kastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J.
Affiliations: Johns Hopkins University (US)
National Cancer Institute (US)
Massachusetts Institute of Technology (US)
ORCID: Kastan, Michael B.
Zhan, Qimin
Carrier, France
Jacks, Tyler
Vogelstein, Bert
Fornace, Albert J.
Venue: Cell
Publisher: Elsevier BV
Published: 1992-11
Volume: 71
Issue: 4
Pages: 587-597
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/0092-8674(92)90593-2
OpenAlex: W1986179131
Cited by: 3,047
References: 64
Citations by year: 2026: 11 · 2025: 16 · 2024: 17 · 2023: 20 · 2022: 23 · 2021: 23 · 2020: 24 · 2019: 16 · 2018: 31 · 2017: 34 · 2016: 35 · 2015: 43 · 2014: 44 · 2013: 30 · 2012: 48
FWCI: 86.58
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (CA 09071, CA43460, T32CA009071)
National Institute of Environmental Health Sciences (ES05777)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
Keywords: ataxia telangiectasia, p53, GADD45, cell cycle checkpoints, G1/S checkpoint, ionizing radiation, DNA damage response, cell cycle arrest, signal transduction, cancer susceptibility, radiosensitivity
MeSH terms: Amino Acid Sequence, Animals, Ataxia Telangiectasia, Base Sequence, Cell Cycle, Cell Line, Cloning, Molecular, DNA Damage, DNA Repair, Gene Expression Regulation, Humans, Molecular Sequence Data, Genes, p53, Mutagenesis, Mice

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A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

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