For example, in 2002, Masanori Takahashi, currently Professor at Graduate School of Medicine Osaka University and colleagues suggested that muscle stiffness, a cardinal feature of DM, was caused by decrease in
chloride channel proteins due to mis - splicing, but the cause of heart arrhythmia has been unknown for a long time.
Not exact matches
Scientists create compounds called «correctors» to fix the CFTR
proteins so that proper amounts transit to the cell surface where they can serve as
chloride channels to help maintain a well - hydrated airway.
The study of these models shows that
proteins MCL1 and GlialCAM play a crucial role in localization and regulation of
chloride channel CLC - 2 in the glia, and proves that the
channel is involved in the disease.
But if the mutant CF
protein had been elevated to the cell surface by a corrector candidate drug, then genistein, as the doorman, would open the
channel and allow
chloride in and out, making the cells glow blue.
A CFTR
protein with this mutation can not fold properly and can not navigate its way to the surface of the cell where it would normally reside, providing a
channel for
chloride to flow in and out.