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Calmin (CLMN) is a single-pass type IV transmembrane protein containing calponin homology domains, primarily localized to the endoplasmic reticulum (ER) tubules where it functions as an ER–actin molecular tether[3][1]. CLMN anchors ER tubules to actin cytoskeletal structures (notably at focal adhesions), facilitating adhesion disassembly and cell motility[1]. Its actin-regulating domains are required for actin association, while its transmembrane region is required for ER localization. Loss of CLMN affects actin organization, impairs focal adhesion turnover, and disrupts cell migration. In addition to roles in cytoskeletal dynamics, CLMN has been associated with cell cycle exit during neuronal differentiation, suggesting possible tissue-specific functions. No direct links to therapeutic targeting, interacting drugs, biomarker utility, or safety concerns are currently reported for this protein[1][3].
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