@article{oai:shiga-med.repo.nii.ac.jp:00003860,
 author = {森宗, 孝夫 and 田埜, 郁実 and 田中, 雄也 and 雪上, 晴加 and 山元, 武文 and 遠山, 育夫 and 丸尾, 良浩 and 西村, 正樹 and 森, 雅樹 and MORIMUNE, Takao and TANO, Ayami and TANAKA, Yuya and YUKIUE, Haruka and YAMAMOTO, Takefumi and TOOYAMA, Ikuo and MARUO, Yoshihiro and NISHIMURA, Masaki and MORI, Masaki},
 issue = {4},
 journal = {PLoS ONE},
 month = {Apr},
 note = {pdf, It is not fully understood how enzymes are regulated in the tiny reaction field of a cell. Several enzymatic proteins form cytoophidia, a cellular macrostructure to titrate enzymatic activities. Here, we show that the epileptic encephalopathy-associated protein Tbc1d24 forms cytoophidia in neuronal cells both in vitro and in vivo. The Tbc1d24 cytoophidia are distinct from previously reported cytoophidia consisting of inosine monophosphate dehydrogenase (Impdh) or cytidine-5'-triphosphate synthase (Ctps). Tbc1d24 cytoophidia is induced by loss of cellular juvenescence caused by depletion of Gm14230, a juvenility-associated lncRNA (JALNC) and zeocin treatment. Cytoophidia formation is associated with impaired enzymatic activity of Tbc1d24. Thus, our findings reveal the property of Tbc1d24 to form cytoophidia to maintain neuronal cellular juvenescence., Journal Article},
 title = {Gm14230 controls Tbc1d24 cytoophidia and neuronal cellular juvenescence.},
 volume = {16},
 year = {2021}
}