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The Quest for Protectors of Genomic Stability

Courtesy of Linda B. Schultz CHECK POINT: The 53Bp1-dependent checkpoint pathway. DNA double-strand breaks are caused by irradiation and other geotoxic events. The ATM [ataxia-telangiectasia mutated] molecule phosphorylates H2AX at or near the break, an event required for 53Bp1 phosphorylation and localization into nuclear foci. Nearly 15 years ago, Saccharomyces cerevisiae researchers at the University of Washington discovered the function of Rad9, the first DNA damage-checkpoint protei

Linda Schultz
Courtesy of Linda B. Schultz
 CHECK POINT: The 53Bp1-dependent checkpoint pathway. DNA double-strand breaks are caused by irradiation and other geotoxic events. The ATM [ataxia-telangiectasia mutated] molecule phosphorylates H2AX at or near the break, an event required for 53Bp1 phosphorylation and localization into nuclear foci.

Nearly 15 years ago, Saccharomyces cerevisiae researchers at the University of Washington discovered the function of Rad9, the first DNA damage-checkpoint protein.1 The finding's im-portance was not lost on cancer researchers: The Rad9 protein protects cells from genomic instability, a hallmark of cancer cells, by delaying progression into the cell cycle until DNA is repaired. Since then, numerous mammalian homologs of these checkpoint proteins have been identified, including ataxia telangiectasia mutated (ATM), which responds swiftly to a critical type of DNA damage--the double-strand break (DSB)--by phosphorylating key proteins in numerous signaling pathways.2 But a big question, until now, had remained unanswered: What regulates...

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