Excited to see this study, in collaboration with the De Camilli group @pdc-lab.bsky.social, published in its final format! We resolved the structure of VPS13C and found that it adopts a lipid-transfer-incompetent conformation. We also show that CaM binds VPS13s and may help regulate their function.
cell.com
Cryo-EM structure of soluble VPS13C suggests its regulation by a conformational switch and by calmodulin
VPS13C, whose dysfunction causes Parkinson’s disease, adopts a lipid-transfer-inactive
conformation in the cytoplasm and relies on calmodulin for proper folding and localization
to membrane surfaces.
