Fig. 2
From: The cell cycle checkpoint inhibitors in the treatment of leukemias
DNA damages sensor and mediators in the response to DSBs and SSBs. DNA damages trigger the recruitment of specific damage sensor protein complexes. On one hand, the MRN (MRE11–RAD50–NBS1) complex is required for the activation of ataxia-telangiectasia mutated (ATM) in response to double-strand breaks (DSBs). On the other hand, the ATM- and Rad3-related (ATR)-interacting protein (ATRIP) complex, formed by ATR-ATRIP-9-1-1 complex, is recruited to sites of single-strand breaks and activates ATR. The activation of ATM and ATR promotes respectively the activation of two different effectors, CHK2 and CHK1. Although currently, the activator of WEE1 is unknown, it is believed that CHK1 promotes WEE1 activation