ReviewFEBS letters2026
Regulation of CFTR stability at the plasma membrane-Mechanisms and therapeutic opportunities in cystic fibrosis.
Review in FEBS letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
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Authors and funding
2 authors.
Funding
Abstract
CFTR stability at the plasma membrane is controlled by a dynamic balance between trafficking, endocytosis, recycling, and degradation. Interactions with scaffold proteins such as NHERF1 and ezrin anchor CFTR to the actin cytoskeleton, reducing mobility and enhancing stability. Cytoskeletal dynamics, regulated by GTPases like RhoA, Rac1, and Rap1, further influence CFTR retention and function. Phosphorylation by kinases including PKA, LMTK2, and SYK modulates channel activity and membrane presence. Whereas rescue of F508del-CFTR with modulators can rescue its defective folding and premature degradation, reduced membrane stability persists. Overall, understanding the molecular mechanisms governing CFTR regulation provides critical insights for developing more effective treatments targeting its stability and function in cystic fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.