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ATM (Ataxia telangiectasia mutated) and ATR (Ataxia telangiectasia and Rad3 related) are closely related kinases that are activated by DNA damage. They are serine-threonine protein kinases which are part of the phosphatidylinositol 3' kinase-like kinase (PIKK) enzyme family.
|Cat No||Product Name / Activity|
|Potent and selective ATR kinase inhibitor; antitumor|
|Potent and selective ATM kinase inhibitor|
|Potent ATM kinase inhibitor|
|MRN-ATM pathway inhibitor|
ATM (Ataxia telangiectasia mutated) and ATR (Ataxia telangiectasia and Rad3 related) are closely related kinases that are activated by DNA damage. These serine-threonine protein kinases are part of the phosphatidylinositol 3' kinase-like kinase (PIKK) family.
Upon recruitment by the DNA damage binding proteins/complexes (ATRIP for ATR; MRN for ATM), ATM/ATR initiate the DNA damage checkpoint by phosphorylating a number of key proteins. Once activated, the checkpoint leads to cell cycle arrest and either DNA repair or apoptosis. ATM is activated by double stranded breaks and phosphorylates Chk2, whilst ATR is activated by single strand breaks and phosphorylates Chk1.
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.