Eduard Stefan

This study identifies a catalytically inactive PKCα mutation that drives chordoid glioma by rewiring cellular interactions and impairing cell junction function.

This study uses KinCon-reporter technology to analyze conformational changes in disease-associated kinases upon drug, regulatory protein, and pathway activation interactions, revealing insights into therapeutic strategies.

The paper identifies missense variants in NF2 that affect its conformation and tumor suppressor function through systematic mutational interaction perturbation analysis.

RO_SCPLOWESISTORC_SCPLOW predicts resistance mutations by optimizing four criteria using Pareto frontiers, identifying clinically relevant mutations in EGFR and BRAF inhibitors.