Fibroblast growth factor 13 (FGF13)

Fibroblast growth factor 13 (FGF13) is a member of the FGF11 subfamily, also known as FGF homologous factors (FHFs), which are structurally related to canonical FGFs but do not typically act via FGF receptors in a paracrine manner[1][3]. FGF13 is a non-secreted, intracellular protein prominently expressed in developing and mature neurons of the central and peripheral nervous systems, as well as cardiac tissue[1][3]. Functionally, it binds directly to tubulin, thereby promoting microtubule polymerization and stabilization, which is crucial for neuronal differentiation, migration, and proper cortical development[2][1]. FGF13 can also interact with voltage-gated sodium channels (Na_v), influencing their function and, consequently, neuronal excitability and cardiac conduction[1]. Mutations in FGF13 cause various human neurological disorders, including X-linked intellectual disabilities and possibly Börjeson-Forssman-Lehmann syndrome[1][3]. Recent work suggests FGF13 might be secreted under stress and activate classical FGF signaling pathways, although its primary role is intracellular[1]. No drugs are currently approved that directly target FGF13; instead, its loss results in disease phenotypes, and its essential roles pose challenges for therapeutic modulation[1].

Other names

FHF2FGF-13FHF-2FLJ30672Fibroblast growth factor homologous factor 2DEE90LINC00889XLID110

Not classically drug-targetable; physiologic activity involves intracellular binding to tubulin and modulating sodium channels, rather than ligand-receptor interactions. Experimental data suggest FGF13 may be secreted under stress and could potentially activate FGFRs (fibroblast growth factor receptors) to trigger downstream signaling in certain contexts[1]