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Friction on mucosal surfaces" refers to the resistance encountered when two mucosal surfaces slide against one another, a property principally determined by the structure, hydration, and molecular constituents (notably mucins) of the mucosa. While there are key molecules (such as MUC1 and other mucins) that reduce friction by acting as natural lubricants, 'friction on mucosal surfaces' itself is an emergent biophysical characteristic, not a protein, receptor, or druggable biological target[1][2][3]. Therefore, it is not considered a therapeutic target, though understanding and modulating this property is important in areas such as biomaterials, oral health, and regenerative medicine. The molecular basis for low friction involves mucins—heavily glycosylated proteins that form a protective, hydrated layer over epithelial surfaces[1][3]. These mucins, especially MUC1, function to retain water, form gels, and reduce wear on epithelia, thus lowering friction forces[1][3]. No drugs directly "target" friction per se, though some therapies aim to modify mucin production or properties to improve lubrication in disease states. The entry "Friction on mucosal surfaces" is therefore a **descriptor of a physiological process** and not a valid entry in a list of molecular targets.
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