Advillin (AVIL)

Advillin (AVIL) is an actin-binding protein that belongs to the gelsolin/villin superfamily and is structurally similar to villin[1][3]. It is highly and specifically expressed in peripheral sensory neurons, where it plays a key role in neurite outgrowth, axonal regeneration, and neuronal plasticity, particularly during development and following injury[1]. Advillin is required for normal cytoskeletal remodeling and cell motility, interacting with other proteins such as SREC-I[1]. \n\nPathologically, AVIL is strongly overexpressed in glioblastoma, promoting tumor cell proliferation, migration, and oncogenic transformation; patients with higher tumoral AVIL have worse prognosis[2]. AVIL’s oncogenic effects operate through actin cytoskeleton modulation and a signaling axis involving stabilization of FOXM1 and upregulation of LIN28B, converging on let-7 miRNA suppression[2]. Mutations that disrupt AVIL’s actin-bundling capacity are also linked to steroid-resistant nephrotic syndrome, likely by disturbing cytoskeletal regulation in kidney cells[1][2]. \n\nAdvillin is not a classical therapeutic target like a receptor, enzyme, or transporter; rather, it is a cytoskeletal regulator essential for neuronal differentiation but aberrantly drives transformation and disease when dysregulated[1][2][3]. No direct therapeutic drugs targeting AVIL are currently described; rather, AVIL’s function as a disease marker and regulator of downstream oncogenic pathways is of primary importance in research contexts[2].

Other names

p92FLJ12386ADVILDOC6NPHS21advillin