Enabled homolog (ENAH) (ENAH)

Enabled homolog (ENAH), also known as ENAH actin regulator or mammalian enabled, is a member of the Ena/VASP family of actin regulatory proteins. ENAH orchestrates actin cytoskeletal dynamics, directly regulating actin filament assembly and cellular processes such as cell motility, adhesion, and morphology. ENAH’s expression and splicing are tightly controlled, with certain isoforms linked to the maintenance of epithelial traits as well as the epithelial-to-mesenchymal transition critical during cancer metastasis. High levels of ENAH and its splice variants are associated with aggressive tumor behavior, serving as prognostic markers in breast and colorectal cancers. Beyond oncology, ENAH is essential for autophagy, axon guidance, and maintaining cardiac cell architecture. Its activity is regulated by interaction partners (e.g., adaptor proteins, kinases) and post-translational modifications. Experimental peptides with high specificity have been developed to study ENAH function, but no therapeutic drugs are currently available that selectively target this protein

Other names

MENAMammalian enabledhMenaFLJ10773NDPP1Mena delta 11aENAprotein enabled homologenabled homolog (Drosophila)

Not standardly targeted by drugs; experimental binders (e.g., PCARE-based) selectively engage the ENAH EVH1 domain to block ENAH-dependent cell adhesion and possibly invasion