The mechanism by which Chtop expression is controlled via an autoregulatory negative feedback loop has been established. The results provide a mechanism for maintaining the cellular level of Chtop by intron retention and nonsense-mediated decay of its own mRNA, which will facilitate the development of therapeutic reagents for the treatment of glioblastoma and severe anemia including β-thalassemias and sickle cell disease.
Program Information
JST CREST
Research Area “Structural Life Science and Advanced Core Technologies for Innovative Life Science Research”
Research Theme “Molecular studies of RNA-dysmetabolic syndrome – From ribonucleoproteomics to structural life science –”
Journal Information
Keiichi Izumikawa, Harunori Yoshikawa, Hideaki Ishikawa, Yuko Nobe, Yoshio Yamauchi, Sjaak Philipsen, Richard J Simpson, Toshiaki Isobe, and Nobuhiro Takahashi. “Chtop (Chromatin target of Prmt1) auto-regulates its expression level via intron retention and nonsense-mediated decay of its own mRNA”. Nucleic Acids Research, the open-access journal of Oxford University Press, Published online 28 September 2016, doi: 10.1093/nar/gkw831.
Contact
[About Research]
Nobuhiro Takahashi, Ph.D.
Professor, Graduate School of Agriculture, Tokyo University of Agriculture & Technology
E-mail: 
URL: http://old-www.tuat.ac.jp/en/index.html
[About Program]
Tetsu Kawaguchi
Life Innovation Group, Department of Innovation Research, JST
E-mail: 