Damage to DNA strands resulting in breakage can lead to chromosomal translocation, uncontrolled cellular growth and cancer. These breaks can occur following exposure to agents such as ionizing radiation, or in programmed events such as gene shuffling. In mammalian cells this damage is repaired by a family of proteins involved in non-homologous end joining (NHEJ).

In August 9 Nature, John Walker and colleagues at the Memorial Sloan-Kettering Cancer Center, New York report the structure of the Ku heterodimer, a well known DNA repair protein and the nature of it's interaction with the DNA double strands (Nature 2001, 412:607-614).

Walker et al. employed X-ray crystallography to observe the Ku-DNA complex and multiple wavelength anomalous diffraction to look at the Ku heterodimer itself. This confirmed that the protein was composed of two subunits — Ku70 and Ku80. Previous studies have shown that both Ku70 and Ku80 knock-outs result...

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