A. N. Economides

The paper shows that ActA forms non-signaling complexes with ACVR1 that are trafficked to lysosomes and degraded, unlike Activin B, AC, and AB which remain on the surface.

This study shows that ACVR1 antibodies, intended to block ACVR1 activation, instead stimulate heterotopic ossification in FOP by activating FOP-mutant ACVR1 through dimerization.

The paper shows that the non-signaling complex formed by Activin A and ACVR1 reduces disease severity in FOP by tempering heterotopic ossification.

This study demonstrates that targeted enzyme replacement therapy using antibody-enzyme fusion proteins improves skeletal muscle phenotypes in Pompe disease mice compared to standard enzyme replacement therapy.