Functional coupling of chloride-proton exchanger ClC-5 to gastric H+,K+-ATPase
about
Genetic Ablation of the ClC-2 Cl- Channel Disrupts Mouse Gastric Parietal Cell Acid Secretion.Overexpression of the Endosomal Anion/Proton Exchanger ClC-5 Increases Cell Susceptibility toward Clostridium difficile Toxins TcdA and TcdB.Insulin is involved in transcriptional regulation of NKCC and the CFTR Cl(-) channel through PI3K activation and ERK inactivation in renal epithelial cells.The Mechanistic Links between Insulin and Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Cl- Channel.The asparagine 533 residue in the outer pore loop region of the mouse PKD2L1 channel is essential for its voltage-dependent inactivation.
P2860
Functional coupling of chloride-proton exchanger ClC-5 to gastric H+,K+-ATPase
description
2014 nî lūn-bûn
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2014年の論文
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2014年論文
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2014年論文
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2014年論文
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2014年論文
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2014年論文
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2014年论文
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2014年论文
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2014年论文
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name
Functional coupling of chloride-proton exchanger ClC-5 to gastric H+,K+-ATPase
@en
type
label
Functional coupling of chloride-proton exchanger ClC-5 to gastric H+,K+-ATPase
@en
prefLabel
Functional coupling of chloride-proton exchanger ClC-5 to gastric H+,K+-ATPase
@en
P2093
P2860
P356
P1433
P1476
Functional coupling of chloride-proton exchanger ClC-5 to gastric H+,K+-ATPase
@en
P2093
Akira Ikari
Hideki Sakai
Hisato Sakamoto
Ichiro Naito
Kazuhiro Tsukada
Koji Manabe
Kyosuke Fujita
Sei Sasaki
Shinichi Uchida
Taiga Higuchi
P2860
P356
10.1242/BIO.20136205
P577
2014-01-15T00:00:00Z