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• W2122860488 abstract "The most frequent mutant variant of the cystic fibrosis transmembrane conductance regulator (CFTR), ΔF508‐CFTR, is misprocessed and subsequently degraded in the endoplasmic reticulum. Using the patch‐clamp technique, we showed that co‐expressions of ΔF508‐CFTR with the N‐terminal CFTR truncates containing bi‐arginine (RXR) retention/retrieval motifs result in a functional rescue of the ΔF508‐CFTR mutant channel in COS‐1 cells. This ΔF508‐CFTR rescue process was strongly impaired when truncated CFTR constructs possessed either the ΔF508 mutation or arginine‐to‐lysine mutations in RXRs. In conclusions, our data demonstrated that expression of truncated CFTR constructs could be a novel promising approach to improve maturation of ΔF508‐CFTR channels." @default.
• W2122860488 created "2016-06-24" @default.
• W2122860488 creator A5037895771 @default.
• W2122860488 creator A5064463193 @default.
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• W2122860488 date "2003-10-15" @default.
• W2122860488 modified "2023-10-14" @default.
• W2122860488 title "Rescue of functional ΔF508-CFTR channels by co-expression with truncated CFTR constructs in COS-1 cells" @default.
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• W2122860488 doi "https://doi.org/10.1016/s0014-5793(03)01162-1" @default.
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