Atm selectively regulates distinct p53-dependent cell-cycle checkpoint and apoptotic pathways
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Summary
The results support a model in which upstream effectors such as Atm selectively activate p53 to regulate specific downstream pathways, providing a mechanism for controlling distinct cell-cycle and apoptotic responses.
- Type
- article
- Published
- 1997-12-01
- Cited by
- 137
- References
- 31
- OpenAlex
- https://openalex.org/W2070019711
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:25910365
Keywords
Cell cycle, Apoptosis, Cell cycle checkpoint, Biology, Cell biology
References
- Analysis of the ATM protein in wild-type and ataxia telangiectasia cells.
- Antibodies: A Laboratory Manual
- Participation of p53 protein in the cellular response to DNA damage.
- Dual roles of ATM in the cellular response to radiation and in cell growth control.
- The ataxia-telangiectasia gene product, a constitutively expressed nuclear protein that is not up-regulated following genome damage.
- Radiation-induced cell cycle arrest compromised by p21 deficiency
- Ataxia telangiectasia mutant protein activates c-Abl tyrosine kinase in response to ionizing radiation
- The Product of the ATM Gene Is a 370-kDa Nuclear Phosphoprotein*
- A novel form of Epstein-Barr virus latency in normal B cells in vivo.
- A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia.
- Differential induction of transcriptionally active p53 following UV or ionizing radiation: defects in chromosome instability syndromes?
- Sequence-specific transcriptional activation is essential for growth suppression by p53.
- WAF1, a potential mediator of p53 tumor suppression.
- atm and p53 cooperate in apoptosis and suppression of tumorigenesis, but not in resistance to acute radiation toxicity
- Improved method for computing potential doubling time from flow cytometric data.
- Tumor suppressor p53 is a direct transcriptional activator of the human bax gene.
- Atm-deficient mice: a paradigm of ataxia telangiectasia.
- Thymocyte apoptosis induced by p53-dependent and independent pathways
- p53 is required for radiation-induced apoptosis in mouse thymocytes
- Tumor spectrum analysis in p53-mutant mice.
Cited by
- The catalytic subunit of DNA-dependent protein kinase selectively regulates p53-dependent apoptosis but not cell-cycle arrest.
- Molecular evolution of the p53 network in reptiles
- Correction of prototypic ATM splicing mutations and aberrant ATM function with antisense morpholino oligonucleotides
- ATM dependent apoptosis in the nervous system
- β-elemene enhances both radiosensitivity and chemosensitivity of glioblastoma cells through the inhibition of the ATM signaling pathway.
- Atm-, p53-, and Gadd45a-deficient mice show an increased frequency of homologous recombination at different stages during development.
- ATM: genome stability, neuronal development, and cancer cross paths.
- Ionizing Radiation-Induced DNA Damage, Response, and Repair
- Abnormal myo-inositol and phospholipid metabolism in cultured fibroblasts from patients with ataxia telangiectasia.
- Caffeine Sensitizes Human H358 Cell Line to p53-mediated Apoptosis by Inducing Mitochondrial Translocation and Conformational Change of BAX Protein*
- Induction of the TRAIL receptor KILLER/DR5 in p53-dependent apoptosis but not growth arrest
- Chk2 is dispensable for p53-mediated G1 arrest but is required for a latent p53-mediated apoptotic response
- Apoptosis regulators and their role in tumorigenesis.
- Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs.
- Mechanisms of p53-mediated apoptosis
- Drosophila p53 is a structural and functional homolog of the tumor suppressor p53.
- The cellular response to p53: the decision between life and death
- Roles of BRCA1 and its interacting proteins
- Hereditäre Karzinomsyndrome in der Frauenheilkunde
- Gene amplification in fibroblasts from ataxia telangiectasia (AT) patients and in X-ray hypersensitive AT-like Chinese hamster mutants.
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