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Abrogation of glucosidase I–mediated glycoprotein deglucosylation results in a sick phenotype in fission yeasts: Model for the human MOGS-CDG disorder

Glucosidase I (GI) removes the outermost glucose from protein-linked Glc(3)Man(9)GlcNAc(2) (G3M9) in the endoplasmic reticulum (ER). Individuals with congenital disorders of glycosylation MOGS-CDG bear mutations in the GI-encoding gene (gls1). Although GI absence has been reported to produce lethali...

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Podrobná bibliografie
Vydáno v:	J Biol Chem
Hlavní autoři:	Gallo, Giovanna L., Valko, Ayelén, Aramburu, Sofía I., Etchegaray, Emiliana, Völker, Christof, Parodi, Armando J., D'Alessio, Cecilia
Médium:	Artigo
Jazyk:	Inglês
Vydáno:	American Society for Biochemistry and Molecular Biology 2018
Témata:	Glycobiology and Extracellular Matrices
On-line přístup:	https://ncbi.nlm.nih.gov/pmc/articles/PMC6311512/ https://ncbi.nlm.nih.gov/pubmed/30389790 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1074/jbc.RA118.004844
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Abrogation of glucosidase I–mediated glycoprotein deglucosylation results in a sick phenotype in fission yeasts: Model for the human MOGS-CDG disorder

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