Ying-Hsin Chen

Abstract INTRODUCTION RESULTS DISCUSSION MATERIALS AND METHODS Acknowledgments Supplementary Materials REFERENCES Information & Authors Metrics & Citations View Options References Figures Tables Media Share This article has 0 eLetter . Abstract Duchenne muscular dystrophy (DMD) is a fatal disorder caused by loss of dystrophin, a protein essential for muscle cell integrity. To date, no therapeutic has restored full-length dystrophin.

Research Article Robert Buschauer1,*, Yoshitaka Matsuo2,*, Takato Sugiyama2, Ying-Hsin Chen3, Najwa Alhusaini3, Thomas Sweet3, Ken Ikeuchi1,2, Jingdong Cheng1, Yasuko Matsuki2, Risa Nobuta2, Andrea Gilmozzi1, Otto Berninghausen1, Petr Tesina1, Thomas Becker1, Jeff Coller3,†, Toshifumi Inada2,†, Roland Beckmann1,† 1Gene Center and Department of Biochemistry, University of Munich, 81377 Munich, Germany. 2Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, Japan.

Coupling translation and mRNA decay Gene expression requires messenger RNAs (mRNAs)—DNA-derived blueprints of genes—to be translated by protein-producing ribosomes. The levels of mRNAs are tightly regulated, in part by controlling their half-lives. In eukaryotic cells, mRNA half-life is largely linked to translational efficiency, but the mechanism underlying this link has remained elusive. Buschauer et al.