@article{oai:kanazawa-u.repo.nii.ac.jp:00027370,
 author = {小林, 昌彦 and 山本, 健一 and Ishikawa, Kazuhiro and Ishii, Hideshi and Murakumo, Yoshiki and Mimori, Koshi and Kobayashi, Masahiko and Yamamoto, Ken-ichi and Mori, Masaki and Nishino, Hiroshi and Furukawa, Yusuke and Ichimura, Keiichi},
 journal = {BMC Molecular Biology},
 month = {Apr},
 note = {Background Previous studies suggest that human RAD9 (hRad9), encoding a DNA damage checkpoint molecule, which is frequently amplified in epithelial tumor cells of breast, lung, head and neck cancer, participates in regulation of the tumor suppressor p53-dependent transactivation of pro-survival P21WAF1. This study examined the exact mechanism of the hRad9 function, especially through the phosphorylation of the C-terminus, in the transcription regulation of P21WAF1. Results The transfection of phosphorylation-defective hRAD9 mutants of C-terminus resulted in reduction of the p53-dependent P21WAF1 transactivation; the knockdown of total hRad9 elicited an increased P21WAF1 mRNA expression. Immunoprecipitation and a ChIP assay showed that hRad9 and p53 formed a complex and both were associated with two p53-consensus DNA-binding sequences in the 5' region of P21WAF1 gene. The association was reduced in the experiment of phosphorylation-defective hRAD9 mutants. Conclusion The present study indicates the direct involvement of hRad9 in the p53-dependent P21WAF1 transcriptional mechanism, presumably via the phosphorylation sites, and alterations of the hRad9 pathway might therefore contribute to the perturbation of checkpoint activation in cancer cells., 金沢大学がん研究所がん分子細胞制御},
 title = {Rad9 modulates the P21WAF1 pathway by direct association with p53},
 volume = {8},
 year = {2007}
}