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A single amino acid substitution in CFTR converts ATP to an inhibitory ligand.
Lin, Wen-Ying; Jih, Kang-Yang; Hwang, Tzyh-Chang.
Afiliação
  • Lin WY; Department of Medical Pharmacology and Physiology, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO 65211 Department of Medical Pharmacology and Physiology, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO 65211.
  • Jih KY; Department of Medical Pharmacology and Physiology, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO 65211 Physician-Scientist Program, National Yang-Ming University, Taipei, 112 Taiwan.
  • Hwang TC; Department of Medical Pharmacology and Physiology, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO 65211 Department of Medical Pharmacology and Physiology, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO 65211 hwangt@health.missouri.edu.
J Gen Physiol ; 144(4): 311-20, 2014 Oct.
Article em En | MEDLINE | ID: mdl-25225552
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Trifosfato de Adenosina / Regulador de Condutância Transmembrana em Fibrose Cística Idioma: En Revista: J Gen Physiol Ano de publicação: 2014 Tipo de documento: Article
Texto completo
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Trifosfato de Adenosina / Regulador de Condutância Transmembrana em Fibrose Cística Idioma: En Revista: J Gen Physiol Ano de publicação: 2014 Tipo de documento: Article