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Cited by 146

Loss of motoneuron-specific microRNA-218 causes systemic neuromuscular failure

Amin, Neal D., Bai, Ge, Klug, Jason R., Bonanomi, Dario, Pankratz, Matthew T., Gifford, Wesley D., Hinckley, Christopher A., Sternfeld, Matthew J. +5 more·2015·Science
DOI 10.1126/science.aad2509PMC PMC4913787
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Abstract

The makings of motor neuron disease: Developing motor neurons link the muscles to the central nervous system. Amin et al. found that microRNA-218 (miR-218) was expressed in developing motor neurons and repressed a wide network of genes whose expression typifies other sorts of neurons. Mice lacking miR-218 died at birth with symptoms characteristic of human motor neuron diseases. Science , this issue p. 1525

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Crossref · 10.1126/science.aad2509

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  • Genetic deletion of both miR-218 loci in mice results in embryonic inability to form functional neuromuscular junctions and ultimately motor neuron degeneration.

    “Genetic deletion of both miR-218 loci in mice resulted in embryonic inability to form functional neuromuscular junctions and, ultimately, MN degeneration (Amin et al., 2015).”

    From MicroRNA Profiling Reveals Marker of Motor Neuron Disease in ALS Models (2017) · cites this paper as Amin et al., 2015

  • The MN-enrichment of miR-218 has been established previously in developing MNs and was found to be important for MN function.

    “The MN-enrichment of one of these miRNAs (miR-218) has been established previously in developing MNs and was found to be important for MN function (Amin et al., 2015;Thiebes et al., 2015).”

    From MicroRNA Profiling Reveals Marker of Motor Neuron Disease in ALS Models (2017) · cites this paper as Amin et al., 2015

  • miR-218 is indispensable for embryonic motor neurons.

    “and is indispensable for embryonic MNs (Amin et al., 2015).”

    From MicroRNA Profiling Reveals Marker of Motor Neuron Disease in ALS Models (2017) · cites this paper as Amin et al., 2015

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Research works printed but not linked: 28

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Cited by

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Authors
Amin, N. D., Bai, G., Klug, J. R., Bonanomi, D., Pankratz, M. T., Gifford, W. D., Hinckley, C. A., Sternfeld, M. J., Driscoll, S. P., Dominguez, B., Lee, K.-F., Jin, X., & Pfaff, S. L.
Affiliations
  • Howard Hughes Medical Institute and Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
  • Molecular Neurobiology Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
  • Peptide Biology Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
2015-12-18
Volume
350
Issue
6267
Pages
1525-1529
ISSN
  • 0036-8075
  • 1095-9203
DOI
10.1126/science.aad2509
PMC
PMC4913787
Cited by
146
References
3
Language
en
Licence
www.sciencemag.org/about/science-licenses-journal-article-reuse (vor, 366 d)
Funders
  • Howard Hughes Medical Institute
  • National Cancer Institute (P30 CA014195)
  • National Institute of Neurological Disorders and Stroke (NINDS) (P30 NS072031)
  • NINDS (F31-NS080340-03)
  • H.A. and Mary K. Chapman Charitable Foundation
  • Leona M. and Harry B. Helmsley Charitable Trust
  • UCSD Medical Scientist Training Program (T32-GM007198)
  • Marshall Heritage Foundation
  • Sol Goldman Trust
  • The Clayton Foundation

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