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• W2067265556 abstract "The clinical course of Cystic Fibrosis is characterized by recurrent pulmonary infections which ultimately lead to death by respiratory failure. The most common CF causing mutation, deltaF508-CFTR, produces an incorrectly folded protein, which accumulates within the endoplasmic reticulum. However, the molecular mechanism by which the deltaF508-CFTR protein facilitates pulmonary infection and inflammation remains unclear. Here we show that the expression of deltaF508-CFTR causes a constitutive activation of the pro-inflammatory transcription factor NF-kappaB by eliciting an ER stress reaction, the ER-overload response. This endogenous NF-kappaB activation stimulates the transcription of pro-inflammatory cytokines thereby commencing an inflammatory cascade within the CF lung." @default.
• W2067265556 created "2016-06-24" @default.
• W2067265556 creator A5013314518 @default.
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• W2067265556 creator A5069668576 @default.
• W2067265556 date "2002-01-15" @default.
• W2067265556 modified "2023-09-30" @default.
• W2067265556 title "ΔF508-CFTR Causes Constitutive NF-κB Activation through an ER-Overload Response in Cystic Fibrosis Lungs" @default.
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• W2067265556 doi "https://doi.org/10.1515/bc.2002.029" @default.
• W2067265556 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11934265" @default.
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