ΔF508 CFTR Pool in the Endoplasmic Reticulum Is Increased by Calnexin Overexpression

The most common cystic fibrosis transmembrane conductance regulator (CFTR) mutant in cystic fibrosis patients, ΔF508 CFTR, is retained in the endoplasmic reticulum (ER) and is consequently degraded by the ubiquitin-proteasome pathway known as ER-associated degradation (ERAD). Because the prolonged i...

Täydet tiedot

Bibliografiset tiedot

Julkaisussa:	Mol Biol Cell
Päätekijät:	Okiyoneda, Tsukasa, Harada, Kazutsune, Takeya, Motohiro, Yamahira, Kaori, Wada, Ikuo, Shuto, Tsuyoshi, Suico, Mary Ann, Hashimoto, Yasuaki, Kai, Hirofumi
Aineistotyyppi:	Artigo
Kieli:	Inglês
Julkaistu:	American Society for Cell Biology 2004
Aiheet:	Articles
Linkit:	https://ncbi.nlm.nih.govhttps://pmc.ncbi.nlm.nih.gov/articles/PMC329241/ https://ncbi.nlm.nih.govhttps://pubmed.ncbi.nlm.nih.gov/14595111/ https://ncbi.nlm.nih.govhttps://doi.org/10.1091/mbc.E03-06-0379
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