The Paradoxical Signals of Two TrkC Receptor Isoforms Supports a Rationale for Novel Therapeutic Strategies in ALS

@inproceedings{Brahimi2016ThePS,
  title={The Paradoxical Signals of Two TrkC Receptor Isoforms Supports a Rationale for Novel Therapeutic Strategies in ALS},
  author={Fouad Brahimi and Mario Maira and Pablo F. Barcelona and Alba S{\'a}nchez Gal{\'a}n and Tahar Aboulkassim and Katrina A Teske and Mary-Louise Rogers and Lisa N. Bertram and Jing Wang and Masoud Yousefi and Robert Archer Rush and Marc R Fabian and Neil Cashman and H Uri Saragovi},
  booktitle={PloS one},
  year={2016}
}
Full length TrkC (TrkC-FL) is a receptor tyrosine kinase whose mRNA can be spliced to a truncated TrkC.T1 isoform lacking the kinase domain. Neurotrophin-3 (NT-3) activates TrkC-FL to maintain motor neuron health and function and TrkC.T1 to produce neurotoxic TNF-α; hence resulting in opposing pathways. In mouse and human ALS spinal cord, the reduction of miR-128 that destabilizes TrkC.T1 mRNA results in up-regulated TrkC.T1 and TNF-α in astrocytes. We exploited conformational differences to… CONTINUE READING

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