Increased surface p2x4 receptors by mutant sod1 proteins contribute to als pathogenesis in sod1-g93a mice

HIGHLIGHTS

• who: Elu00e9onore Bertin from the UnivBordeaux, CNRS, IMN, UMR, Bordeaux, France Institute of Immunology, University Medical Center have published the research work: Increased surface P2X4 receptors by mutant SOD1 proteins contribute to ALS pathogenesis in SOD1-G93A mice, in the Journal: (JOURNAL)
• what: The authors show that several ALS-related misfolded proteins including mutants of or TDP-43 lead to a significant increase in surface P2X4 density and function in vitro. The authors demonstrate in the the of SOD1-G93A (SOD1) that misfolded SOD1-G93A proteins directly interact with endocytic protein-2 (AP2); thus acting . . .
  

   

  

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