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Mouse K-Cl cotransporter KCC1: cloning, mapping, pathological expression, and functional regulation.
Oral magnesium supplements reduce erythrocyte dehydration in patients with sickle cell disease.
Hypoxia activates a Ca2+-permeable cation conductance sensitive to carbon monoxide and to GsMTx-4 in human and mouse sickle erythrocytes.
Structure and genetic polymorphism of the mouse KCC1 gene.
Disruption of erythroid K-Cl cotransporters alters erythrocyte volume and partially rescues erythrocyte dehydration in SAD mice.
Therapy with oral clotrimazole induces inhibition of the Gardos channel and reduction of erythrocyte dehydration in patients with sickle cell disease.
Inhibition of Ca(2+)-dependent K+ transport and cell dehydration in sickle erythrocytes by clotrimazole and other imidazole derivatives.
Novel therapies for prevention of erythrocyte dehydration in sickle cell anemia.
Treatment with oral clotrimazole blocks Ca(2+)-activated K+ transport and reverses erythrocyte dehydration in transgenic SAD mice. A model for therapy of sickle cell disease.
A new therapeutic approach for sickle cell disease. Blockade of the red cell Ca(2+)-activated K+ channel by clotrimazole.
Harnessing red cell membrane pathophysiology towards point-of-care diagnosis for sickle cell disease.
Anemia, Sickle Cell
RBC Ion Transporters as Hemoglobinopathy Risk Modifiers
Sickle Red Cell K+ Transporter Genetics in S. cerevisiae
CLOTRIMAZOLE THERAPY TO INHIBIT CYST ENLARGEMENT IN PKD
Genome-wide association study of erythrocyte density in sickle cell disease patients.
Combined genetic disruption of K-Cl cotransporters and Gardos channel KCNN4 rescues erythrocyte dehydration in the SAD mouse model of sickle cell disease.
Corrigendum to "Combined genetic disruption of K-Cl cotransporters and Gardos channel KCNN4 rescues erythrocyte dehydration in the SAD mouse model of sickle cell disease" [Blood Cells Mol. Dis. (2019) start page-end page not yet assigned] https://doi.org/10.1016/j.bcmd.2019.102346.
Anemia Sickle Cell