Combined genetic disruption of K-Cl cotransporters and Gardos channel KCNN4 rescues erythrocyte dehydration in the SAD mouse model of sickle cell disease-Reference-Cited by-同舟云学术

Combined genetic disruption of K-Cl cotransporters and Gardos channel KCNN4 rescues erythrocyte dehydration in the SAD mouse model of sickle cell disease

Published:2019-11 Issue: Volume:79 Page:102346
ISSN:1079-9796
Container-title:Blood Cells, Molecules, and Diseases
language:en
Short-container-title:Blood Cells, Molecules, and Diseases

Author:

Shmukler Boris E.,Rivera Alicia,Bhargava Parul,Nishimura Katherine,Hsu Ann,Kim Edward H.,Trudel Marie,Rust Marco B.,Hubner Christian A.,Brugnara Carlo,Alper Seth L.

Funder

NIH

Publisher

Elsevier BV

Subject

Cell Biology,Hematology,Molecular Biology,Molecular Medicine

Reference26 articles.

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3. Physiological roles of the intermediate conductance, Ca2+-activated potassium channel Kcnn4;Begenisich;J. Biol. Chem.,2004

4. Lineage-specific BCL11A knockdown circumvents toxicities and reverses sickle phenotype;Brendel;J. Clin. Invest.,2016

5. Ca(2+)-activated K+ transport in erythrocytes. Comparison of binding and transport inhibition by scorpion toxins;Brugnara;J. Biol. Chem.,1993

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