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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Dotu, Ivan Ishimura, Ryuta Zhou, Huihao Senju, Satoru Chuang, Jeffrey H. Ackerman, Susan L. Nagy, Gabor Yang, Xiang-lei Schimmel, Paul Nishimura, Yasuharu |
| Description | Author Affiliation: Ishimura R ( Howard Hughes Medical Institute and The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.); Nagy G ( Howard Hughes Medical Institute and The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.); Dotu I ( The Jackson Laboratory for Genomic Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA.); Zhou H ( The Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.); Yang XL ( The Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.); Schimmel P ( The Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.); Senju S ( Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University, Honjo 1-1-1, Chuo-ku, Kumamoto 860-8556, Japan.); Nishimura Y ( Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University, Honjo 1-1-1, Chuo-ku, Kumamoto 860-8556, Japan.); Chuang JH ( The Jackson Laboratory for Genomic Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA.); Ackerman SL ( Howard Hughes Medical Institute and The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA. susan.ackerman@jax.org.) |
| Abstract | In higher eukaryotes, transfer RNAs (tRNAs) with the same anticodon are encoded by multiple nuclear genes, and little is known about how mutations in these genes affect translation and cellular homeostasis. Similarly, the surveillance systems that respond to such defects in higher eukaryotes are not clear. Here, we discover that loss of GTPBP2, a novel binding partner of the ribosome recycling protein Pelota, in mice with a mutation in a tRNA gene that is specifically expressed in the central nervous system causes ribosome stalling and widespread neurodegeneration. Our results not only define GTPBP2 as a ribosome rescue factor but also unmask the disease potential of mutations in nuclear-encoded tRNA genes. |
| ISSN | 00368075 |
| e-ISSN | 10959203 |
| Journal | Science |
| Issue Number | 6195 |
| Volume Number | 345 |
| Language | English |
| Publisher | American Association for the Advancement of Science (United States) |
| Publisher Date | 2014-07-25 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cell Cycle Proteins Metabolism Cerebellum GTP-Binding Proteins Microfilament Proteins Neurodegenerative Diseases Genetics Protein Biosynthesis RNA, Transfer, Arg Ribosomes Animals Cell Nucleus Pathology Mice Mice, Inbred BALB C Mice, Inbred C57BL Point Mutation RNA Splice Sites Research Support, American Recovery And Reinvestment Act Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | History and Philosophy of Science |
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