Zobrazeno 1 - 10
of 168
pro vyhledávání: '"Tzyh Chang Hwang"'
Autor:
Xiaolong Gao, Han-I Yeh, Zhengrong Yang, Chen Fan, Fan Jiang, Rebecca J. Howard, Erik Lindahl, John C. Kappes, Tzyh-Chang Hwang
Publikováno v:
Nature Communications, Vol 15, Iss 1, Pp 1-13 (2024)
Abstract Loss-of-function mutations of the CFTR gene cause the life-shortening genetic disease cystic fibrosis (CF), whereas overactivity of CFTR may lead to secretory diarrhea and polycystic kidney disease. While effective drugs targeting the CFTR p
Externí odkaz:
https://doaj.org/article/86b783d0ca63434bb3730316e05145d3
Publikováno v:
Frontiers in Molecular Biosciences, Vol 9 (2022)
Cystic fibrosis (CF) is a lethal hereditary disease caused by loss-of-function mutations of the chloride channel cystic fibrosis transmembrane conductance regulator (CFTR). With the development of small-molecule CFTR modulators, including correctors
Externí odkaz:
https://doaj.org/article/4e430ee905ab43e39072ecb308e8adb4
Autor:
Winnie Khor, Tzyh-Chang Hwang, Chih-Chien Wang, Aliaksandr A. Yarmishyn, Jiunn-Tyng Yeh, Shih-Hwa Chiou, Shih-Jie Chou
Publikováno v:
Stem Cell Research, Vol 60, Iss , Pp 102683- (2022)
Cystic fibrosis (CF) is a genetic disease affects CFTR channel synthesis. While 90 percent of the CF patients now benefit from small molecule target therapies, this treatment has yet to extend to those bearing nonsense mutations. Studies of these rar
Externí odkaz:
https://doaj.org/article/d320ba5238754044b926d5f68138bc5b
Publikováno v:
Journal of Cystic Fibrosis
Journal of Cystic Fibrosis, 2022, ⟨10.1016/j.jcf.2022.09.010⟩
Journal of Cystic Fibrosis, 2022, ⟨10.1016/j.jcf.2022.09.010⟩
International audience; The root cause of cystic fibrosis (CF), the most common life-shortening genetic disease in the Caucasian population, is the loss of function of the CFTR protein, which serves as a phosphorylation-activated, ATP-gated anion cha
Autor:
Gert de Wilde, Maarten Gees, Sara Musch, Katleen Verdonck, Mia Jans, Anne-Sophie Wesse, Ashvani K. Singh, Tzyh-Chang Hwang, Thierry Christophe, Mathieu Pizzonero, Steven Van der Plas, Nicolas Desroy, Marlon Cowart, Pieter Stouten, Luc Nelles, Katja Conrath
Publikováno v:
Frontiers in Pharmacology, Vol 10 (2019)
The deletion of phenylalanine at position 508 (F508del) in cystic fibrosis transmembrane conductance regulator (CFTR) causes a severe defect in folding and trafficking of the chloride channel resulting in its absence at the plasma membrane of epithel
Externí odkaz:
https://doaj.org/article/8d68380c55104f5f99c3962f9d0c136b
Autor:
Maarten Gees, Sara Musch, Steven Van der Plas, Anne-Sophie Wesse, Ann Vandevelde, Katleen Verdonck, Oscar Mammoliti, Tzyh-Chang Hwang, Kathleen Sonck, Pieter Stouten, Andrew M. Swensen, Mia Jans, Jan Van der Schueren, Luc Nelles, Martin Andrews, Katja Conrath
Publikováno v:
Frontiers in Pharmacology, Vol 9 (2018)
There is still a high unmet need for the treatment of most patients with cystic fibrosis (CF). The identification and development of new Cystic Fibrosis Transmembrane conductance Regulator (CFTR) modulators is necessary to achieve higher clinical ben
Externí odkaz:
https://doaj.org/article/99852fe337bc4182a943b73d103f71f5
Publikováno v:
PLoS ONE, Vol 13, Iss 12, p e0209862 (2018)
Cystic fibrosis transmembrane conductance regulator (CFTR), the culprit behind the genetic disease cystic fibrosis (CF), is a phosphorylation-activated, but ATP-gated anion channel. Studies of human CFTR over the past two decades have provided an in-
Externí odkaz:
https://doaj.org/article/e6c4c1118f51469ba91e3b394fc2e79b
Publikováno v:
Handbook of experimental pharmacology.
People with cystic fibrosis (CF) suffer from a multi-organ disorder caused by loss-of-function variants in the gene encoding the epithelial anion channel cystic fibrosis transmembrane conductance regulator (CFTR). Tremendous progress has been made in
Autor:
Winnie Khor, Tzyh-Chang Hwang, Chih-Chien Wang, Aliaksandr A. Yarmishyn, Jiunn-Tyng Yeh, Shih-Hwa Chiou, Shih-Jie Chou
Publikováno v:
Stem Cell Research, Vol 60, Iss, Pp 102683-(2022)
Cystic fibrosis (CF) is a genetic disease affects CFTR channel synthesis. While 90 percent of the CF patients now benefit from small molecule target therapies, this treatment has yet to extend to those bearing nonsense mutations. Studies of these rar