Talk:CH391L/S2013 Logan R Myler Jan 30 2013

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(New page: '''Tanya Raymond''' ATM is able to phosphorylate H2AX, but so is ATR and DNA-PK. [1] Do you have any speculation as to why, upon DNA-PK inhibition, there was only...)
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'''[[User:Tanya_E_Raymond|Tanya Raymond]]'''  ATM is able to phosphorylate H2AX, but so is ATR and DNA-PK. [1] Do you have any speculation as to why, upon DNA-PK inhibition, there was only diminished phosphorylation signal in the presence of MDC1 tethering?
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'''[[User:Tanya_E_Raymond|Tanya Raymond]]'''  ATM is able to phosphorylate H2AX, but so is ATR and DNA-PK. [1] Can you speculate as to why, upon DNA-PK inhibition, there was only diminished phosphorylation signal in the presence of MDC1 tethering?
1. Monika Podhorecka, Andrzej Skladanowski, and Przemyslaw Bozko, “H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy,” Journal of Nucleic Acids, vol. 2010, Article ID 920161, 9 pages, 2010. doi:10.4061/2010/920161
1. Monika Podhorecka, Andrzej Skladanowski, and Przemyslaw Bozko, “H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy,” Journal of Nucleic Acids, vol. 2010, Article ID 920161, 9 pages, 2010. doi:10.4061/2010/920161

Revision as of 16:18, 31 January 2013

Tanya Raymond ATM is able to phosphorylate H2AX, but so is ATR and DNA-PK. [1] Can you speculate as to why, upon DNA-PK inhibition, there was only diminished phosphorylation signal in the presence of MDC1 tethering?

1. Monika Podhorecka, Andrzej Skladanowski, and Przemyslaw Bozko, “H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy,” Journal of Nucleic Acids, vol. 2010, Article ID 920161, 9 pages, 2010. doi:10.4061/2010/920161

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