Roman R. Schlimgen

This study reveals an unconventional activation mechanism of the atypical GPCR ACKR3 using engineered nanobodies and cryo-EM, showing that extracellular pocket volume changes, not microswitch conformational shifts, drive receptor activity.

This study uses inverse agonistic nanobodies to reveal constitutive activity of ACKR3, showing it drives non-canonical signaling and basal cell motility, suggesting therapeutic potential.

The paper investigates how G6PD variants affect red blood cell storage, transfusion performance, and recipient physiology using multiple datasets and experimental models.