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EC Number	General Information	Commentary	Reference
2.3.1.78	physiological function	mutation of a putative LYPXnL-based binding site within HGSNAT for the V-domain of ALIX ablates association of HGSNAT with ALIX, posttranslational maturation, and transport through the endolysosomal network. A mutation within the V-domain of ALIX demonstrates enhanced HGSNAT association. HGSNAT still coimmunoprecipitates with truncations of ALIX lacking the V-domain. Knockdown of ALIX does not inhibit HGSNAT trafficking through the endo-lysosomal network	756105

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Release 2023.1 (January 2023)