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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Amino-terminal domain of ATRIP contributes to intranuclear relocation of the ATR-ATRIP complex following DNA damage.

ATM and rad3-related protein kinase ( ATR), a member of the phosphoinositide kinase-like protein kinase family, plays a critical role in cellular responses to DNA structural abnormalities in conjunction with its interacting protein, ATRIP. Here, we show that the amino-terminal portion of ATRIP is relocalized to DNA damage-induced nuclear foci in an RPA-dependent manner, despite its lack of ability to associate with ATR. In addition, ATR-free ATRIP protein can be recruited to the nuclear foci. Our results suggest that the N-terminal domain of the ATRIP protein contributes to the cell cycle checkpoint by regulating the intranuclear localization of ATR.[1]

References

  1. Amino-terminal domain of ATRIP contributes to intranuclear relocation of the ATR-ATRIP complex following DNA damage. Itakura, E., Takai, K.K., Umeda, K., Kimura, M., Ohsumi, M., Tamai, K., Matsuura, A. FEBS Lett. (2004) [Pubmed]
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