ATM in focus

a damage sensor and cancer target

Hilal S. Khalil, Hemanth Tummala, Nikolai Zhelev

Research output: Contribution to journalArticle

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Abstract

The ability of a cell to conserve and maintain its native DNA sequence is fundamental for the survival and normal functioning of the whole organism and protection from cancer development. Here we review recently obtained results and current topics concerning the role of the ataxia-telangiectasia mutated (ATM) protein kinase as a damage sensor and its potential as therapeutic target for treating cancer. This monograph discusses DNA repair mechanisms activated after DNA double-strand breaks (DSBs), i.e. non-homologous end joining, homologous recombination and single strand annealing and the role of ATM in the above types of repair. In addition to DNA repair, ATM participates in a diverse set of physiological processes involving metabolic regulation, oxidative stress, transcriptional modulation, protein degradation and cell proliferation. Full understanding of the complexity of ATM functions and the design of therapeutics that modulate its activity to combat diseases such as cancer necessitates parallel theoretical and experimental efforts. This could be best addressed by employing a systems biology approach, involving mathematical modelling of cell signalling pathways.
Original languageEnglish
Number of pages60
JournalBioDiscovery
Volume5
Issue number1
DOIs
Publication statusPublished - 30 Nov 2012

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Ataxia Telangiectasia
DNA Repair
Ataxia Telangiectasia Mutated Proteins
Physiological Phenomena
Neoplasms
Systems Biology
Double-Stranded DNA Breaks
Homologous Recombination
Protein Kinases
Proteolysis
Oxidative Stress
Cell Proliferation
Therapeutics

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Khalil, Hilal S. ; Tummala, Hemanth ; Zhelev, Nikolai. / ATM in focus : a damage sensor and cancer target. In: BioDiscovery. 2012 ; Vol. 5, No. 1.
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ATM in focus : a damage sensor and cancer target. / Khalil, Hilal S.; Tummala, Hemanth; Zhelev, Nikolai.

In: BioDiscovery, Vol. 5, No. 1, 30.11.2012.

Research output: Contribution to journalArticle

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