Shinako Araki

TL;DR: It is reported that induction of sCLU is delayed, peaking 72 h after low doses of ionizing radiation, and is dependent on the up-regulation of insulin-like growth factor-1 as well as phosphorylation-dependent activation of its receptor (IGF-1 and IGF-1R, respectively).

TL;DR: It is reported that TGF-beta1-activated SMA- and MAD3 (Smad3/4) transcription factors specifically bound to the second promoter region of HDM2, leading to increasedHDM2 protein expression and destabilization of p53 in human cancer cell lines.

TL;DR: It is hypothesized that activation of the TGF-beta signaling pathway, which often occurs after IR exposure, can in turn activate the CLU promoter, and thus represent a potential link between IR-induced adaptive responses, genomic instability and bystander effects.

TL;DR: This work shows that activation of Ataxia telangiectasia-mutated kinase (ATM) by endogenous or exogenous forms of DNA damage was required to relieve basal repression of IGF-1 transcription by the p53/NF-YA complex, leading to sCLU expression.

TL;DR: It is shown that depletion of endogenous nCLU protein using siRNA specific to its truncated mRNA increased clonogenic survival of ionizing radiation (IR)-exposed cells and may explain recent clinical results showing that highly malignant tumors have lost the ability to accumulate n CLU levels, thereby avoiding growth inhibition and cell death.