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Publication : The Mammalian-Specific Protein Armcx1 Regulates Mitochondrial Transport during Axon Regeneration.

First Author  Cartoni R Year  2016
Journal  Neuron Volume  92
Issue  6 Pages  1294-1307
PubMed ID  28009275 Mgi Jnum  J:293776
Mgi Id  MGI:6453783 Doi  10.1016/j.neuron.2016.10.060
Citation  Cartoni R, et al. (2016) The Mammalian-Specific Protein Armcx1 Regulates Mitochondrial Transport during Axon Regeneration. Neuron 92(6):1294-1307
abstractText  Mitochondrial transport is crucial for neuronal and axonal physiology. However, whether and how it impacts neuronal injury responses, such as neuronal survival and axon regeneration, remain largely unknown. In an established mouse model with robust axon regeneration, we show that Armcx1, a mammalian-specific gene encoding a mitochondria-localized protein, is upregulated after axotomy in this high regeneration condition. Armcx1 overexpression enhances mitochondrial transport in adult retinal ganglion cells (RGCs). Importantly, Armcx1 also promotes both neuronal survival and axon regeneration after injury, and these effects depend on its mitochondrial localization. Furthermore, Armcx1 knockdown undermines both neuronal survival and axon regeneration in the high regenerative capacity model, further supporting a key role of Armcx1 in regulating neuronal injury responses in the adult central nervous system (CNS). Our findings suggest that Armcx1 controls mitochondrial transport during neuronal repair.
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