Experimental evolution of yeast models of congenital disorders of glycosylation reveals that reduction, but not loss, of phosphoglucomutase activity best compensates for impaired phosphomannomutase activity.

High-throughput animal tracking and quantitative behaviour analysis detects diverse phenotypes in genetic disease models at a scale that makes drug screens possible.

Impairment of protein N-glycosylation disrupts neural cell adhesion mediated by highly glycosylated members of the IgSF-CAM protein family.

Mannose phosphate isomerase is a metabolic enzyme regulating cell survival in both embryonic and cancer cells.