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SLC26A9 as a Potential Modifier and Therapeutic Target in Cystic Fibrosis Lung Disease

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Summary: SLC26A9 is identified as the primary source of constitutive anion secretion across bronchial epithelium, showing differential responses to common inhibitors of anion secretion compared to CFTR. These results should lay a strong foundation for future studies exploring the activation of SLC26A9 as an alternative anion channel in cystic fibrosis, and investigating how single-nucleotide polymorphisms in SLC26A9 modulate airway disease.

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Summary: SLC26A9 is a constitutively active Cl- transporter that contributes to epithelial Cl- secretion and is implicated in respiratory disorders such as CF. Studies have shown that enhancing SLC26A9 expression can increase CFTR function and response to CFTR correctors, suggesting its potential as a therapeutic target for CF.

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