@article{oai:nagasaki-u.repo.nii.ac.jp:00017068,
 author = {Matsuse, Michiko and Saenko, Vladimir and Sedliarou, Ilya and Rogounovitch, Tatiana and Nakazawa, Yuka and Mitsytake, Norisato and Akulevich, Natallia and Namba, Hiroyuki and Yamashita, Shunichi},
 issue = {1},
 journal = {Journal of Radiation Research},
 month = {Jan},
 note = {Thyroid hormone receptors (THRs) widely govern cell growth, differentiation and metabolism acting in a ligand- and cofactor-dependent manner to modulate tissue-specific gene expression. Given a large variety of genes regulated by THRs and multiplicity of cellular processes potentially influenced by THRs, we addressed the role of THRB (thyroid hormone receptor beta) in cellular radiosensitivity. Wild-type and mutant THRB were overexpressed in several cell lines using an adenovirus-mediated gene delivery and their effects were examined after cell exposure to γ-rays. Wild-type THRB decreased clonogenic survival of the cell lines with low levels of endogenous THRB, retarded their growth and synergized with radiation in decreasing proliferative potential and promoting cellular senescence. These changes were accompanied by the accumulation of p21 (CDKN1A, CIP1, WAF1) and p16 (CDKN2A, INK4a) inhibitors of cyclindependent kinases and by the decrease of Rb (retinoblastoma protein) phosphorylation. Mutant THRB produced a radioprotective effect, attenuated radiation-induced growth inhibition and cellular senescence. The results suggest that THRB may modulate cellular radiosensitivity and stress-induced senescence., 長崎大学学位論文 学位記番号:博（医歯薬）甲第148号 博士（医学）学位授与年月日:平成20年3月19日, Journal of Radiation Research, 49(1), pp.17-27; 2008},
 pages = {17--27},
 title = {A Novel Role for Thyroid Hormone Receptor Beta in Cellular Radiosensitivity},
 volume = {49},
 year = {2008}
}