Latest Cystic fibrosis transmembrane conductance regulator Stories
ChanTest is a world leader in drug safety and discovery, in areas particularly relevant to Cystic Fibrosis. Cleveland, OH (PRWEB) September 11, 2013
A little more than a year after the FDA approved Kalydeco (Vx-770), the first drug of its kind to treat the underlying cause of cystic fibrosis, University of Missouri researchers believe they have found exactly how this drug works and how to improve its effectiveness in the future.
A recent study led by Gergely Lukacs, a professor at McGill University's Faculty of Medicine, Department of Physiology, and published in the January issue of Cell, has shown that restoring normal function to the mutant gene product responsible for cystic fibrosis (CF) requires correcting two distinct structural defects.
Cystic fibrosis (CF), a chronic disease that clogs the lungs and leads to life-threatening lung infections, is caused by a genetic defect in a chloride channel called cystic fibrosis transmembrane conductase regulator (CFTR).
When researchers discovered the primary genetic defect that causes cystic fibrosis (CF) back in 1989, they opened up a new realm of research into treatment and a cure for the disease.
Researchers have identified an unconventional path that may correct the defect underlying cystic fibrosis.
Researchers at the University of North Carolina at Chapel Hill School of Medicine have demonstrated that the gene mutated in cystic fibrosis not only controls traffic on the chloride highway, but also keeps the sodium highway from being overused.
Crosstalk between ion channels points to new therapeutic strategy, Penn study finds.
Investigators report new findings about its special relationship with pH levels inside cells.
Researchers at the University of North Carolina at Chapel Hill have discovered a genetic risk factor for severe liver disease in people with cystic fibrosis.