Christopher T. Schafer

The paper designs miniproteins that selectively block or bias chemokine receptor signaling by targeting CCL25, demonstrating their ability to suppress CCR9 and modulate ACKR4 responses.

This study compares the conformational dynamics of ACKR3 and CXCR4 using MD simulations and BRET assays, revealing that ACKR3's dynamic behavior leads to activation-proneness and G protein-incompetence.

This study shows ACKR4 is phosphorylated by GRK3 without needing G protein activation, through a unique receptor motif that recruits the kinase directly.

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.

This study identifies an arrestin-independent phosphorylation mechanism that terminates CCR9 signaling, revealing a novel regulatory pathway for GPCR function.