Iain M. Hay

This study reveals the structural basis of a phosphoinositide-driven mTORC2-AKT positive feedback loop through cryo-EM structures and functional analysis.

The paper traces the origin of four synchronous renal tumours in a child to an early embryonic MTOR mutation, showing its role in tumour development and clinical implications.

The paper identifies how Afadin is recruited to PTPRK via its pseudophosphatase domain, revealing that substrate specificity is determined by interactions outside the active site.