Figures & data
Figure 1 PIKK family members,
Notes: The PIKK family members have a C-terminal protein kinase domain flanked on either side by an N-terminal FAT-domain and a C-terminal FAT-C domain with PIKK regulatory domain (PRD). The N-termini are largely composed of HEAT repeats.
Abbreviations: ATM, ataxia-telangiectasia mutated gene; FAT, FRAP, ATM, TRRAP; HEAT, Huntingtin, elongation factor 3, protein phosphatase 2A, and yeast kinase TOR.
Abbreviations: ATM, ataxia-telangiectasia mutated gene; FAT, FRAP, ATM, TRRAP; HEAT, Huntingtin, elongation factor 3, protein phosphatase 2A, and yeast kinase TOR.
Figure 2 Activation of ATM.
Notes: (A) Schematic of the ATM protein with domain organization. (B) Activation of ATM by DNA damage or hypotonic stress requires the Mre11 complex, or ATMIN, respectively. Activated ATM is monomeric, phosphorylated and acetylated. Alternatively, ATM is activated directly by ROS to form disulfide bridge-mediated dimer.
Abbreviations: Ac, acetylation; ATM, ataxia-telangiectasia mutated gene; ATMIN, ATM interacting protein-acting as mediator of ATM activation in response to hypotonic stress or chloroquine treatment; FAT, FRAP, ATM, TRRAP; HEAT, Huntingtin, elongation factor 3, protein phosphatase 2A, and yeast kinase TOR; P, phosphorylation; ROS, Reactive Oxygen Species; SS, disulfide bridge between the two monomeric ATM protein molecules.
Abbreviations: Ac, acetylation; ATM, ataxia-telangiectasia mutated gene; ATMIN, ATM interacting protein-acting as mediator of ATM activation in response to hypotonic stress or chloroquine treatment; FAT, FRAP, ATM, TRRAP; HEAT, Huntingtin, elongation factor 3, protein phosphatase 2A, and yeast kinase TOR; P, phosphorylation; ROS, Reactive Oxygen Species; SS, disulfide bridge between the two monomeric ATM protein molecules.
