ATR

Our genome experiences a moderate amount of DNA damage in our cells on a daily basis.  This DNA damage can be in response to external environmental factors, or be a result of our internal metabolic processes going awry.  While normal rates of DNA damage are not an immense threat to our cell processes, DNA damage in critical genes can lead to a variety of disease, including cancer and tumor formation.   After induction of DNA damage (for example, in the form of double strand breaks), phosphorylation and recruitment of the H2AX protein occurs.  This phosphorylation produces gamma H2AX

The p53-binding protein 1 (53BP1) is a DNA damage response factor, which is recruited to nuclear structures at the site of DNA damage.  DNA double-strand breaks (DSBs) are mutations that are detrimental to cell viability and genome stability, and must be repaired either through homologous recombination (HR) or non-homologous end joining (NHEJ). 53BP1 specifically promotes both NHEJ as well as the inhibition of HR repair, yet the decision making on a molecular level between these two routes not clearly understood.