Article
COPII-dependent export of cystic fibrosis transmembrane conductance regulator from the ER uses a di-acidic exit code.
The Journal of cell biology - 11 Oct 2004
Wang Xiaodong, Matteson Jeanne, An Yu, Moyer Bryan, Yoo Jin-San, Bannykh Sergei, Wilson Ian A, Riordan John R, Balch William E
Abstract excerpt
Cystic fibrosis (CF) is a childhood hereditary disease in which the most common mutant form of the CF transmembrane conductance regulator (CFTR) DeltaF508 fails to exit the endoplasmic reticulum (ER). Export of wild-type CFTR from the ER requires the coat complex II (COPII) machinery, as it is sensitive to Sar1 mutants that disrupt normal coat assembly and disassembly. In contrast, COPII is not used to deliver...
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