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Following secretion and self-cleavage of CLCA1, the N-terminal fragment (N-CLCA1) acts in paracrine fashion (1). Dimerization appears to regulate surface trafficking of TMEM16A. N-CLCA1 engages TMEM16A on the cell surface (2), stabilizing TMEM16A dimers, preventing internalization (3) and in turn, results in increased TMEM16A surface expression and calcium-dependent chloride current density.
