James A. McNew

This study uses Drosophila models to identify phospholipid and sphingolipid abnormalities in peroxisomal biogenesis disorders, revealing substrate channeling effects on lipid acyl chain lengths.

The paper shows that increasing neuronal excitability enhances proteomic stress in muscle caused by mutations in the atlastin gene.

The paper shows that the attP40 docking site and its derivatives function as insertional mutations of MSP300, causing phenotypes like nuclear clustering and viability issues.