Shipping Calpastatin to the Rescue: Prevention of Neuromuscular Degeneration through Mitofusin 2.
Level V
Where this comes from
- Record sourced from PubMed, PMID 30282045.
- Also identified by DOI 10.1016/j.cmet.2018.09.017.
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Abstract
How neuromuscular junctions (NMJs) are lost in disease and aging is unclear. Recently in Cell Metabolism, Wang et al. (2018) discovered that endoplasmic reticulum-mitochondria tethering by Mitofusin 2 is required to organize a cleft between these two organelles, which, like a lorry, traffics down the axon to distribute calpastatin to terminals where it blocks NMJ degradation.
Medical subject headings
- Axonal Transport
- Neuromuscular Junction