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Orai1 pore residues control CRAC channel inactivation independently of calmodulin.
Mullins, Franklin M; Yen, Michelle; Lewis, Richard S.
Affiliation
  • Mullins FM; Department of Pathology and Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305 rslewis@stanford.edu fmullins@stanford.edu.
  • Yen M; Department of Pathology and Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305.
  • Lewis RS; Department of Pathology and Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305 rslewis@stanford.edu fmullins@stanford.edu.
J Gen Physiol ; 147(2): 137-52, 2016 Feb.
Article in En | MEDLINE | ID: mdl-26809793
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Full text: 1 Database: MEDLINE Main subject: Calmodulin / Calcium Channels Type of study: Prognostic_studies Limits: Animals / Humans Language: En Journal: J Gen Physiol Year: 2016 Type: Article
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Full text: 1 Database: MEDLINE Main subject: Calmodulin / Calcium Channels Type of study: Prognostic_studies Limits: Animals / Humans Language: En Journal: J Gen Physiol Year: 2016 Type: Article