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ATR is a [[ | ATR is a [[Protein kinase|protein kinase]] enzyme which recognises a range of [[DNA|DNA]] damage and recruits adaptor proteins and more protein kinases ([[Chk1|Chk1]] and [[Chk2|Chk2]]) which then go on to activate repair mechanisms or cause [[Apoptosis|apoptosis]] or [[Cell cycle|cell cycle]] arrest. ATR is [[homologous|homologous]] to [[ATM|ATM]], however ATM only recognises double-stranded DNA breaks whereas ATR can recognise stalled [[Replication forks|replication forks]], damaged [[Nucleotides|nucleotides]], double-stranded breaks and more<ref name="(1)">H. Lodish, C. A. Kaiser, A. Berk, M. Krieger, A. Bretscher, H. Ploegh, A. Amon, M. P. Scott. Molecular Cell Biology. 7th Ed. New York: W. H. Freeman. 2013.</ref>. | ||
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Latest revision as of 15:12, 5 December 2017
ATR is a protein kinase enzyme which recognises a range of DNA damage and recruits adaptor proteins and more protein kinases (Chk1 and Chk2) which then go on to activate repair mechanisms or cause apoptosis or cell cycle arrest. ATR is homologous to ATM, however ATM only recognises double-stranded DNA breaks whereas ATR can recognise stalled replication forks, damaged nucleotides, double-stranded breaks and more[1].
References
- ↑ H. Lodish, C. A. Kaiser, A. Berk, M. Krieger, A. Bretscher, H. Ploegh, A. Amon, M. P. Scott. Molecular Cell Biology. 7th Ed. New York: W. H. Freeman. 2013.