@article{oai:tsukuba.repo.nii.ac.jp:00054766,
 author = {西村, 健 and NISHIMURA, Ken and 永田, 恭介 and NAGATA, Kyosuke and 福田, 綾 and FUKUDA, AYA and 久武, 幸司 and HISATAKE, Koji and Bui, Phuong Linh and Seminario Mondejar, Gonzalo and Kumar, Arun and Aizawa, Shiho and Murano, Kensaku and Hayashi, Yohei and Onuma, Yasuko and Ito, Yuzuru and Nakanishi, Mahito},
 issue = {7},
 journal = {Cell Reports},
 month = {Nov},
 note = {Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) is accompanied by dramatic changes in epigenetic programs, including silencing of endogenous and exogenous retroviruses. Here, we utilized replication-defective and persistent Sendai virus (SeVdp)-based vectors to monitor retroviral silencing during reprogramming. We observed that retroviral silencing occurred at an early reprogramming stage without a requirement for KLF4 or the YY1-binding site in the retroviral genome. Insertional chromatin immunoprecipitation (iChIP) enabled us to isolate factors assembled on the silenced provirus, including components of inhibitor of histone acetyltransferase (INHAT), which includes the SET/TAF-I oncoprotein. Knockdown of SET/TAF-I in mouse embryonic fibroblasts (MEFs) diminished retroviral silencing during reprogramming, and overexpression of template activating factor-I α (TAF-Iα), a SET/TAF-I isoform predominant in embryonic stem cells (ESCs), reinforced retroviral silencing by an SeVdp-based vector that is otherwise defective in retroviral silencing. Our results indicate an important role for TAF-Iα in retroviral silencing during reprogramming.},
 pages = {1909--1922.e5},
 title = {Template Activating Factor-I α Regulates Retroviral Silencing during Reprogramming},
 volume = {29},
 year = {2019},
 yomi = {ニシムラ, ケン and ナガタ, キョウスケ and フクダ, アヤ and ヒサタケ, コウジ}
}