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

Neuron | 2016

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.

Pubmed ID: 28009275 RIS Download

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Associated grants

  • Agency: NEI NIH HHS, United States
    Id: R01 EY021526
  • Agency: NINDS NIH HHS, United States
    Id: R01 NS077929
  • Agency: NICHD NIH HHS, United States
    Id: P30 HD018655
  • Agency: NEI NIH HHS, United States
    Id: P30 EY012196
  • Agency: NICHD NIH HHS, United States
    Id: U54 HD090255
  • Agency: NEI NIH HHS, United States
    Id: R01 EY021242
  • Agency: NIGMS NIH HHS, United States
    Id: R01 GM069808

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