Magali Taulan-Cadars

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The CFTR gene displays a tightly regulated tissue-specific and temporal expression. Mutations in this gene cause cystic fibrosis (CF). In this study we wanted to identify trans-regulatory elements responsible for CFTR differential expression in fetal and adult lung, and to determine the importance of inhibitory motifs in the CFTR-3'UTR with the aim of(More)
PURPOSE Although 97-99% of CFTR mutations have been identified, great efforts must be made to detect yet-unidentified mutations. METHODS We developed a small-scale next-generation sequencing approach for reliably and quickly scanning the entire gene, including noncoding regions, to identify new mutations. We applied this approach to 18 samples from(More)
The promoter of the cystic fibrosis transmembrane conductance regulator gene CFTR is tightly controlled by regulators including CCAAT/enhancer binding proteins (C/EBPs). We previously reported that the transcription factors YY1 and USF2 affect CFTR expression. We can now demonstrate that C/EBPβ, a member of the CCAAT family, binds to the CFTR promoter and(More)
BACKGROUND Although several comprehensive studies have evaluated the role of the CFTR gene in idiopathic diffuse bronchiectasis (DB), it remains controversial. METHODS We analyzed the whole coding region of the CFTR gene, its flanking regions and the promoter in 47 DB patients and 47 controls. Available information about demographic, spirometric,(More)
The development of suitable Cystic Fibrosis (CF) models for preclinical bench tests of therapeutic candidates is challenging. Indeed, the validation of molecules to rescue the p.Phe508del-CFTR channel (encoded by the Cystic Fibrosis Transmembrane conductance Regulator gene carrying the p.Phe508del mutation) requires taking into account their overall effects(More)
Molecular diagnosis of cystic fibrosis is based on the detection of mutation in the CFTR gene, identified in 1989. During the past 20 years, thanks to evolutions of diagnostic techniques, our knowledge of mutation spectrum and pathophysiological mecha‐ nisms involved in the disease has significantly improved. Sanger sequencing and quantitative methods(More)
Impaired airway homeostasis in chronic obstructive pulmonary disease (COPD) could be partly related to club cell secretory protein (CCSP) deficiency. We hypothesize that CCSP G38A polymorphism is involved and aim to examine the influence of the CCSP G38A polymorphism on CCSP transcription levels and its regulatory mechanisms. CCSP genotype and CCSP levels(More)
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