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Arrestin-C (ARR3), also referred to as cone arrestin or X-arrestin, is a member of the arrestin protein family predominantly expressed in cone photoreceptor cells of the vertebrate retina[1][5]. Its primary function is to regulate signal transduction initiated by activation of G protein-coupled receptors (GPCRs) such as cone opsins, facilitating receptor desensitization, endocytosis, and the proper shutoff of visual signaling[1][2][4][5]. Arrestin-C binds activated, phosphorylated forms of cone opsins and plays a key role in returning photoreceptor cells to their baseline state after light exposure[1]. Although crucial for cone cell biology and visual function, Arrestin-C is not currently considered a therapeutic drug target nor is it recognized as a disease biomarker; its dysfunction has not been definitively linked to a major human disease or directly targeted by medicines[1][5]. Arrestin-C is structurally distinct from the non-visual arrestins (arrestin-2/β-arrestin and arrestin-3), which modulate a broader range of GPCR signaling outside the retina[1]. **Notes/Explanation for is_incorrect:** ARR3 is a specific protein but is not considered a classic "therapeutic target" such as a receptor, enzyme, transporter, or ion channel. It is not a canonical receptor or membrane signaling protein but rather an intracellular regulator, mainly in photoreceptor cells. No drugs are known to interact with this protein, and it is not established as a drug target in therapeutic pipelines or clinical trials. Some of the submitted aliases overlap with other arrestins (such as arrestin-3, which refers elsewhere to β-arrestin 2), but ARR3/Arrestin-C specifically denotes cone arrestin, not β-arrestin subtypes[4][5]. Because of overlap with other arrestins and potential confusion with β-arrestin 2 (which *is* sometimes called arrestin-3 in literature but is not ARR3), this entry must be handled with caution, and it is currently **not a validated therapeutic target**.
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