Activation of the ATM kinase by ionizing radiation and phosphorylation of p53.
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- Type
- article
- Published
- 1998-09-11
- Cited by
- 2,194
- References
- 23
- OpenAlex
- https://openalex.org/W2089574530
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:45901669
Keywords
Phosphorylation, DNA-PKcs, Ionizing radiation, Ataxia-telangiectasia, Kinase
References
- DNA-dependent protein kinase is not required for accumulation of p53 or cell cycle arrest after DNA damage.
- Dual roles of ATM in the cellular response to radiation and in cell growth control.
- When is a lipid kinase not a lipid kinase? When it is a protein kinase.
- DNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2.
- A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia.
- The Atr and Atm protein kinases associate with different sites along meiotically pairing chromosomes.
- Cellular localisation of the ataxia-telangiectasia (ATM) gene product and discrimination between mutated and normal forms
- DNA strand breaks: the DNA template alterations that trigger p53-dependent DNA damage response pathways
- V(D)J recombination activates a p53-dependent DNA damage checkpoint in scid lymphocyte precursors.
- Recombinant ATM protein complements the cellular A-T phenotype
- Atm selectively regulates distinct p53-dependent cell-cycle checkpoint and apoptotic pathways
- Mdm2 promotes the rapid degradation of p53
- Phosphorylation of the translational repressor PHAS-I by the mammalian target of rapamycin.
- Fragments of ATM which have dominant-negative or complementing activity
- Overexpression of a kinase‐inactive ATR protein causes sensitivity to DNA‐damaging agents and defects in cell cycle checkpoints
- p53 and ATM: cell cycle, cell death, and cancer.
- DNA damage induces phosphorylation of the amino terminus of p53.
- Defective induction of stress-activated protein kinase activity in ataxia-telangiectasia cells exposed to ionizing radiation.
- A single ataxia telangiectasia gene with a product similar to PI-3 kinase.
- The p53-dependent G1 cell cycle checkpoint pathway and ataxia-telangiectasia.
Cited by
- Discovering inner ear and central auditory system cellular pathways that might contribute to age- related hearing loss
- Oscillations by the p53-Mdm2 feedback loop.
- Critical role for Ser20 of human p53 in the negative regulation of p53 by Mdm2
- Cell cycle control, checkpoint mechanisms, and genotoxic stress.
- Regulation of p53 stability
- The catalytic subunit of DNA-dependent protein kinase selectively regulates p53-dependent apoptosis but not cell-cycle arrest.
- Study of the cytolethal distending toxin (CDT)‐activated cell cycle checkpoint
- ATM-dependent Phosphorylation of Human Rad9 Is Required for Ionizing Radiation-induced Checkpoint Activation*
- Insights into cancer therapeutic design based on p53 and TRAIL receptor signaling
- Effects of hyperthermia on p53 protein expression and activity
- The onset of p53-dependent DNA repair or apoptosis is determined by the level of accumulated damaged DNA.
- Ceramide and Reactive Oxygen Species Generated by H2O2 Induce Caspase-3-independent Degradation of Akt/Protein Kinase B*
- Role of tumor suppressors in DNA damage response.
- Phosphorylation on Thr-55 by TAF1 mediates degradation of p53: a role for TAF1 in cell G1 progression.
- Melanoma cells express elevated levels of phosphorylated histone H2AX foci.
- ATM signaling and 53BP1.
- Identification of Carboxyl-terminal MCM3 Phosphorylation Sites Using Polyreactive Phosphospecific Antibodies*
- ATM sequence variants associate with susceptibility to non‐small cell lung cancer
- ROLE OF ING2 (INHIBITOR OF GROWTH FAMILY MEMBER 2) IN CELLUAR RESPONSES TO DNA DAMAGE
- Mathematical modeling of cell cycle regulation in response to DNA damage: Exploring mechanisms of cell-fate determination
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- Requirement of ATM-dependent phosphorylation of brca1 in the DNA damage response to double-strand breaks.
- Constitutive phosphorylation of IcBa by casein kinase II
- Data from ATM and DNA-PK Function Redundantly to Phosphorylate H2AX after Exposure to Ionizing Radiation
- Data from ATM and DNA-PK Function Redundantly to Phosphorylate H2AX after Exposure to Ionizing Radiation
- Ionizing radiation induces ataxia telangiectasia mutated kinase (ATM)-mediated phosphorylation of LKB1/STK11 at Thr-366.
- The role of ATM and ATR in DNA damage-induced cell cycle control.
- ATM and ATR: sensing DNA damage.