DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation

By C. Bakkenist, M. Kastan. Nature, 2003

3,601 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/7cb4ed1116c1744ed8bb29ceaf31deb69b1b8627

How researchers see this paper

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In Cancer Research

1. J. Bartek
2. Stephen P. Jackson
3. J. Lukas
4. T. de Lange
5. Yosef Shiloh
6. J. Campisi
7. Karlene A. Cimprich
8. C. Lukas

In Molecular Biology

1. Stephen P. Jackson
2. J. Bartek
3. T. de Lange
4. J. Lukas
5. Yosef Shiloh
6. J. Campisi
7. J. Karlseder
8. C. Lukas

In Oncology

1. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. Yosef Shiloh
5. T. de Lange
6. J. Campisi
7. C. Lukas
8. Wilhelm Palm

Citations in the corpus

• Integration of interferon-α/β signalling to p53 responses in tumour suppression and antiviral defence (2003, background): “We infer that, similar to DNA damage, ATM activation is caused by changes in the chromatin structure in virus-infected cell”
• Cell-cycle checkpoints and cancer (2004, background): “The identification of a single, major damage-induced phosphorylation site (serine 1981) led to the demonstration of a new mechanism of ATM regulation that permits a rapid and sensitive switch for checkpoint pathway”
• Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity (2008, background): “DNA strand breaks induced by DNA-damaging agents potently activate ATM and cause its autophosphorylation (30).”
• Cellular response to hyperosmotic stresses. (2007, background): “Multiple agents activate ATM without activating TonEBP/OREBP (124), including urea, UV, IR, and low NaCl (11, 124).”
• Telomeres: protecting chromosomes against genome instability (2010, background): “ATM comes to mind as a molecule that is capable of amplifying damage signals, as it has been suggested that localized damage leads to phosphorylation of most of the ATM molecules in a cell, potentially through changes in chromatin structur”
• ATM and related protein kinases: safeguarding genome integrity (2003, methodology): “A breakthrough in our understanding of this process came in a landmark publication by Bakkenist and Kasta”
• Targeting DNA topoisomerase II in cancer chemotherapy (2009, background): “org/uniprot/Q13315">ATM ) and activation of downstream damage response”
• DNA damage-induced cell death: from specific DNA lesions to the DNA damage response and apoptosis. (2013, background): “This autophosphorylation occurs at Ser1981 [89], which leads to the disassociation of inactive ATM dimers into catalytic active monomers.”
• ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response. (2017, background): “Human ATM phosphorylates itself on S1981, an event proposed to transition the kinase from an inactive dimer into active monomers in response to DNA damage (Bakkenist and Kastan, 2003).”
• The γ‐H2A.X: Is it just a surrogate marker of double‐strand breaks or much more? (2008, methodology): “X was detected after treating (hypotonic treatment, exposure to chloroquine or trichostatin A) cells with chromatin-modifying agents [Bakkenist and Kastan, 2003].”
• Regulation of p53 translation and induction after DNA damage by ribosomal protein L26 and nucleolin. (2005, positive): “Activation of the ATM kinase, as measured by autophosphorylation of Ser1981 (Bakkenist and Kastan, 2003), was not affected by RPL26 overexpression in either unirradiated or irradiated cells (Figure 3A).”