Disruption of the neurotrophin-3 receptor gene trkC eliminates la muscle afferents and results in abnormal movements
Nature, ISSN: 0028-0836, Vol: 368, Issue: 6468, Page: 249-251
1994
- 554Citations
- 107Captures
- 5Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations554
- Citation Indexes554
- 554
- CrossRef504
- Captures107
- Readers107
- 107
- Mentions5
- References5
- Wikipedia5
Article Description
THE trkC gene is expressed throughout the mammalian nervous system and encodes a series of tyrosine protein kinase isoforms that serve as receptors for neurotrophin-3 (NT3), a member of the nerve growth factor (NGF) family of neurotrophic factors. One of these isoforms, gp145/TrkC Kl, mediates the trophic properties of NT3 in cultured cells. Here we show that homozygous mice defective for TrkC tyrosine protein kinase receptors lack la muscle afferent projections to spinal motor neurons and have fewer large myelinated axons in the dorsal root and posterior columns of the spinal cord. These mice display abnormal movements and postures, indicating that NT3/TrkC-dependent sensory neurons may play a primary role in proprioception, the sense of position and movement of the limbs. © 1994 Nature Publishing Group.
Bibliographic Details
Springer Science and Business Media LLC
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