Surachai Supattapone

The paper identifies an alternatively misfolded PrP species, PrPAM, generated by PRNP mutations that may initially protect against prion replication, explaining delayed disease onset.

This study identifies GSK-3β as a regulator of PrPC levels through post-translational mechanisms and shows its impact on PrPSc levels in prion-infected cells.

This paper describes a method to generate infectious prions with site-specific click chemistry modifications for studying prion biology.

This paper introduces a fluorescent non-canonical amino acid to monitor site-specific conformational changes during prion formation and demonstrates its utility in detecting infectious prion conformers.

This study identifies mitochondrial energy production as a key host factor mediating cell death from CSG orthobunyaviruses and shows that reducing energy production can protect cells from viral infection.

The paper identifies core regulators of cell surface PrPC expression through CRISPR screens in neuronal cells, revealing shared and unique regulators in different cell states.

This paper identifies OST complex inhibition as a novel therapeutic approach that reduces prion protein surface expression and prevents prion amplification in both rodent and human prion models.

This study tests anti-prion drugs on knock-in mouse models of inherited prion diseases and finds they do not improve survival or prevent prion accumulation.

This study shows that knock-in mice with specific prion protein mutations spontaneously develop prion disease, producing atypical prion strains with similar properties regardless of mutation type.