title: Rehabilitating mutant GCase.
abstract: Gaucher's disease is a hereditary deficiency of the enzyme β-glucocerebrosidase (GCase) that is most commonly treated by enzyme replacement therapy. In this issue of Chemistry & Biology, Tan and colleagues search for alternative ways to rehabilitate mutant GCase by understanding how it interacts with the proteostasis network.
authors.affiliation: Department of Pharmaceutical Chemistry, Institute for Neurodegenerative Disease, University of California at San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA.
authors.forename: Jennifer N
authors.initials: JN
authors.lastname: Rauch
authors.affiliation: Department of Pharmaceutical Chemistry, Institute for Neurodegenerative Disease, University of California at San Francisco, 675 Nelson Rising Lane, San Francisco, CA 94158, USA. Electronic address: jason.gestwicki@ucsf.edu.
authors.forename: Jason E
authors.initials: JE
authors.lastname: Gestwicki
mesh_terms: D004721:Endoplasmic Reticulum / Q000378:metabolism*; D005776:Gaucher Disease / Q000201:enzymology*; D005962:Glucosylceramidase / Q000235:genetics* / Q000378:metabolism*; D050956:HSP40 Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D050505:Mutant Proteins / Q000378:metabolism*
chemical_list: C494648:DNAJB11 protein, human; D050956:HSP40 Heat-Shock Proteins; D050505:Mutant Proteins; D005962:Glucosylceramidase