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Changing Huntingtin Protein Leads to Improved Neuronal Trafficking

News   Apr 14, 2021 | Original story from UniversitĂ  di Trento

 
Changing Huntingtin Protein Leads to Improved Neuronal Trafficking

In Huntington's Disease, axonal transport is defective and this leads to neuronal degeneration. In this work, we found that the protein mutated in Huntington's Disease, called huntingtin (HTT), needs to be methylated by the enzyme PRMT6 in order to guarantee an efficient axonal transport and the survival of neural cells (in orange and blue we depicted the vesicles that are transported along the axon). Indeed, low PRMT6 levels cause a reduction in the number of vesicles travelling along the axon (top panel), whereas high PRMT6 levels rescue this defect and ameliorate the disease in in vitro and in vivo models (bottom panel). Credit: University of Trento

 
 
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