Miao He

Metabolomic, lipidomic, and N-glycomic analyses of a human cell model of Krabbe disease reveal treatable deficits in glycosylation and serine-ceramide metabolism

Stable isotope tracing is used to comprehensively characterize metabolic perturbations in a human oligodendrocellular Krabbe disease model and suggests impaired protein glycosylation as a previously unrecognized pathogenic mechanism in Krabbe disease.