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Visinin-like protein 1 (VILIP-1) is a neuronal calcium sensor protein encoded by the VSNL1 gene and part of the visinin/recoverin subfamily of EF-hand domain containing calcium-binding proteins[1][4]. It is highly expressed in cerebellar granule cells and modulates intracellular signaling pathways in the central nervous system through a calcium-myristoyl switch, which regulates its association with cellular membranes in response to intracellular calcium changes[1][2]. VILIP-1 plays critical roles in modulating cyclic nucleotide (cAMP/cGMP) signaling by influencing adenylyl cyclase and guanylyl cyclase activity, and it regulates the trafficking and function of key receptors, including nicotinic acetylcholine receptors (particularly the α4β2 subtype), purinergic (P2X2) receptors, and natriuretic peptide receptors[1][2][5]. Functionally, it contributes to synaptic plasticity, neuronal differentiation, cytoskeletal dynamics, and dendritic remodeling. VILIP-1 has been implicated in neurodegenerative diseases such as Alzheimer's, where its levels may serve as a biomarker for neuronal injury[5]. Alternative transcript variants exist, but their full structures are not fully characterized[4]. No direct therapeutic drugs are known to target VILIP-1[1][2][5].
Not applicable (no direct targeting drugs known; mechanism as modulator of signaling pathways via receptor trafficking and cyclic nucleotide regulation)
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