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, which is MAS-dependent and requires an increase of cAMP ( 8 ). Interestingly, we have recently demonstrated that cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated Cl − channel, plays an important role in regulating the
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assuming CFTR modulator therapy. Z-scores of weight, height and BMI were not significantly different between sexes, but they were reduced when compared to the general population. Most patients (68%) had normal glucose tolerance but β cell glucose
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codominant modifier gene for embryonic lethality on mouse proximal chromosome 7 ( 15 ); cystic fibrosis transmembrane conductance regulator null mice ( Cftr M1HSC / Cftr M1HSC ), which usually died of intestinal obstruction similar to that observed in
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mutations. In fact, hundreds of pathogenic gene variants identified in other ethnicities are not causing clinically relevant diseases in Saudis ( 16 ). For instance, mutations in the CFTR gene causing cystic fibrosis in Europeans differ from those
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2561 – 2568 . ( doi:10.1016/j.bbadis.2014.07.012 ) 100 Ivonnet P Salathe M Conner GE. Hydrogen peroxide stimulation of CFTR reveals an Epac-mediated, soluble AC-dependent cAMP amplification pathway common to GPCR signalling . British