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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Han, Sung Min Han, Bingjie Koelle, Michael R. Irving Meyer, Benjamin Baig, Huma S. Lin-moore, Alexander T. Kosmaczewski, Sara Guckian Athar, Wardah Hammarlund, Marc |
| Description | Author Affiliation: Kosmaczewski SG ( Department of Genetics and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510); Han SM ( Department of Genetics and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510); Han B ( Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06510.); Irving Meyer B ( Department of Genetics and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510); Baig HS ( Department of Genetics and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510); Athar W ( Department of Genetics and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510); Lin-Moore AT ( Department of Genetics and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510); Koelle MR ( Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, New Haven, CT 06510.); Hammarlund M ( Department of Genetics and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510); |
| Abstract | Activity of the RNA ligase RtcB has only two known functions: tRNA ligation after intron removal and XBP1 mRNA ligation during activation of the unfolded protein response. Here, we show that RtcB acts in neurons to inhibit axon regeneration after nerve injury. This function of RtcB is independent of its basal activities in tRNA ligation and the unfolded protein response. Furthermore, inhibition of axon regeneration is independent of the RtcB cofactor archease. Finally, RtcB is enriched at axon termini after nerve injury. Our data indicate that neurons have co-opted an ancient RNA modification mechanism to regulate specific and dynamic functions and identify neuronal RtcB activity as a critical regulator of neuronal growth potential. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 27 |
| Volume Number | 112 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2015-07-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Amino Acyl-tRNA Synthetases Metabolism Axons Physiology Caenorhabditis Elegans Proteins Nerve Regeneration RNA Ligase (ATP) RNA, Helminth Genetics Animals Animals, Genetically Modified Axotomy Caenorhabditis Elegans Luminescent Proteins Microscopy, Fluorescence Mutation Neurons RNA, Transfer Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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