Anion Transport Proteins

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  Subject Areas on Research

  • Agonist-induced coordinated trafficking of functionally related transport proteins for water and ions in cholangiocytes. 
  • Angiotensin II acts through the angiotensin 1a receptor to upregulate pendrin. 
  • Bicarbonate-dependent superoxide release and pulmonary artery tone. 
  • Corneal dystrophy mutations R125H and R804H disable SLC4A11 by altering the extracellular pH dependence of the intracellular pK that governs H⁺ (OH^- ) transport. 
  • Deficiency in SLC25A1, encoding the mitochondrial citrate carrier, causes combined D-2- and L-2-hydroxyglutaric aciduria. 
  • Genetic screen of African Americans with Fuchs endothelial corneal dystrophy. 
  • Macrophage invasion contributes to degeneration of stria vascularis in Pendred syndrome mouse model. 
  • Mapping of ionomic traits in Mimulus guttatus reveals Mo and Cd QTLs that colocalize with MOT1 homologues. 
  • Mapping the ankyrin-binding site of the human erythrocyte anion exchanger. 
  • Mapping the binding sites of human erythrocyte ankyrin for the anion exchanger and spectrin. 
  • Mitochondrial ROS Induced Lysosomal Dysfunction and Autophagy Impairment in an Animal Model of Congenital Hereditary Endothelial Dystrophy. 
  • Nutritional modulation of heart failure in mitochondrial pyruvate carrier-deficient mice. 
  • Oxidative stress activates anion exchange protein 2 and AP-1 in airway epithelial cells. 
  • Positive association of SLC26A2 gene polymorphisms with susceptibility to systemic-onset juvenile idiopathic arthritis. 
  • Superoxide-dependent iron uptake: a new role for anion exchange protein 2. 
  • TRANSPORTER OF IBA1 Links Auxin and Cytokinin to Influence Root Architecture. 
  • Targeting the mitochondrial pyruvate carrier attenuates fibrosis in a mouse model of nonalcoholic steatohepatitis. 
  • The molecular identity of the characean OH^- transporter: a candidate related to the SLC4 family of animal pH regulators. 
  • pH dependence of the Slc4a11-mediated H⁺ conductance is influenced by intracellular lysine residues and modified by disease-linked mutations. 
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  Keywords of People

  • Bennett, Vann, George Barth Geller Distinguished Professor of Molecular Biology, Duke Cancer Institute