FOCAL POINT Shichuan Zhang (left, who won the 2010 Marie Curie Award from the Radiation Research Society for his work), Benjamin Chen (right), and colleagues (not shown) generated knockin mice expressing a mutant version of the DNA repair kinase DNA-PKcs that can't be phosphorylated by the upstream kinases ATM and ATR and is therefore unable to activate the nonhomologous end-joining repair pathway. Surprisingly, the mice were also defective in the homologous recombination and Fanconi anemia repair pathways, resulting in chromosome aberrations (far right, arrows) and the death of hematopoietic stem cells. / ZHANG PHOTO COURTESY OF MENGXIA LI; CHEN PHOTO COURTESY OF UT SOUTHWESTERN BIOMEDICAL ART SERVICES

FOCAL POINT Shichuan Zhang (left, who won the 2010 Marie Curie Award from the Radiation Research Society for his work), Benjamin Chen (right), and colleagues (not shown) generated knockin mice expressing a mutant version of the DNA repair kinase DNA-PKcs that can't be phosphorylated by the upstream kinases ATM and ATR and is therefore unable to activate the nonhomologous end-joining repair pathway. Surprisingly, the mice were also defective in the homologous recombination and Fanconi anemia repair pathways, resulting in chromosome aberrations (far right, arrows) and the death of hematopoietic stem cells.

ZHANG PHOTO COURTESY OF MENGXIA LI; CHEN PHOTO COURTESY OF UT SOUTHWESTERN BIOMEDICAL ART SERVICES

This Feature Is Available To Subscribers Only

or Create an Account

Close Modal
Close Modal