Amino‐terminal domain of ATRIP contributes to intranuclear relocation of the ATR–ATRIP complex following DNA damage

Abstract

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.