Lynx1 is a member of the Ly-6/neurotoxin gene superfamily (Lynx family) of proteins that feature a three-looped toxin fold and a cysteine rich motif; structural characteristics that are shared with the snake venom toxin α-bungarotoxin¹.

Lynx1 is expressed in large projection neurons in the hippocampus, cortex, and cerebellum. Initial analysis of the functional consequence of genetic ablation of Lynx1 in mice revealed that Lynx1 is an allosteric modulator of various nicotinic receptors that affects their kinetics, decreases their agonist affinities, and increases their desensitization to overall limit their activation. Lynx1 can serve as a protective measure against neurotoxicity through agonist-induced overstimulation². In fact, deletion of Lynx1 eventually leads to neurodegeneration in aged mice³.

Collectively the findings regarding Lynx1 suggest a direct relationship between plasticity regulation and nicotinic signaling, and underline the significance of fine tuning of nicotinic tone to vastly control the development of brain functions.
Lynx1 activity was shown to be related to the pathophysiology of Alzheimer’s disease as well as cholinergic activity in healthy and tumor cells of bronchial epithelium⁴.