Filip Van Petegem

This study examines how SARS-CoV-2 3CLpro variants maintain catalytic activity despite distant substitutions, revealing structural adaptations that preserve function.

This study uses hiPSC-derived cardiomyocytes to model CRDS, showing that programmed electrical stimulation induces arrhythmias through EADs and re-entry, which can be suppressed by flecainide.

This study identifies rare RYR3 variants causing recurrent rhabdomyolysis by impairing autophagy and mitochondrial function, highlighting RyR3's role in muscle stress adaptation.

This study identifies Cathepsin K as a key host protease for SARS-CoV-2 spike activation and shows it can be inhibited by existing drugs.

This paper introduces REEL-EM, a method combining EELS and single-particle image processing to enable elemental mapping in cryo-preserved macromolecular complexes, demonstrating reliable localization of abundant elements.

This study shows propofol directly binds and inhibits RyR1, reducing Ca2+ release and potentially protecting against malignant hyperthermia.

The paper shows that TBP is not essential for Pol II transcription in mESCs, revealing a TBP-independent mechanism for transcription initiation.