ATR signaling can drive cells into senescence in the absence of DNA breaks

Article Abstract:

A research is done to design a system that would activate ATR in the absence of DNA damage in order to interrogate the contribution of the pathway in the absence of additional signaling cascades that are triggered by genomic lesions. It is concluded that this system adds evidences for the tumor-suppressive potential of the DNA damage response and provides better understanding of specific functions of ATR signaling.

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The fanconi anemia/BRCA pathway: New faces in the crowd

Article Abstract:

The data identifying new components of the Fanconi Anemia (FA) pathway that implecateit in several aspects of the DNA damage response are reviewed. It is shown that abnormalities in the FA pathway are not only found in childhood FA but also in the development of sporadic cancers in adults, where they may influence the response to chemotherapeutic agents.

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ATR couples FANCD2 monoubiquitination to the DNA-damage response

Article Abstract:

A study is conducted to demonstrate that ATR (Ataxia Telangiectasia Mutated and Rad3-related) and RPA1 are required for efficient FANCD2 monoubiquitination. ATR-deficient Seckel syndrome cells form radial chromosomes in response to MMC (Mitomycin C), mimicking the chromosome instability of FA cells is reported.

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