A-type lamins anchor emerin at the inner nuclear membrane via two independent binding sites.

ABSTRACT: Lamins form a dense meshwork at the inner surface of the inner nuclear membrane (INM), where they interact with other nuclear envelope proteins such as emerin. Emerin is an integral membrane protein that is part of the LEM (LAP2/emerin/MAN1) domain family, and mutations in either emerin or lamin A/C can result in Emery-Dreifuss muscular dystrophy and other striated muscle diseases. Emerin is retained at the INM through direct interaction with lamin A/C, and emerin's proper subcellular localization is critical for its ability to influence the mechanical properties of the nucleus and participate in various signaling processes. Nevertheless, the requirements for interaction between emerin and lamin A/C at the INM remain incompletely understood. Here, we report that two distinct regions of lam

SUBMITTER: Odell J 

PROVIDER: S-EPMC12930054 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature