Fasciculation and elongation protein zeta-1 (FEZ1)

Fasciculation and elongation protein zeta-1 (FEZ1) is a human protein encoded by the FEZ1 gene, noted for its vital role in neuronal development, particularly in axonal bundling and elongation, as discovered via its ortholog in C. elegans (unc-76)[1][2][3][7]. FEZ1 acts as a scaffold and adaptor in intracellular transport, especially in the kinesin-1–mediated movement of cargos essential for neuronal function and development[2][3]. It is highly expressed in neuronal tissues, particularly in the developing and adult brain, where it participates in neurite outgrowth, protein trafficking, and the regulation of autophagy[2][3]. Structurally, FEZ1 is largely intrinsically disordered, adopts coiled-coil regions, dimerizes via a disulfide bond, and serves as a hub for various protein-protein interactions[2][3][4]. FEZ1 also interacts with key proteins such as Protein kinase Mζ, Kinesin-1, Munc18, Syntaxin 1a, JIP1, NBR1, DISC1, and others, which underlies its role in both neuronal development and autophagy pathways[1][2][3]. Evidence suggests FEZ1 is involved in antiviral cellular defense, notably restricting infection by HIV[5]. To date, FEZ1 is not a recognized pharmacological target and no drugs are known to directly interact with or modulate its function. However, its dysregulation has been associated with neurodevelopmental and neurodegenerative disorders as well as altered susceptibility to viral infections[2][5].

Other names

UNC-76Zygin IZygin-1STT3A-AS1

Not a direct drug target; no known mechanism of action for drugs