Publication: Mouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins
Mouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins
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Wagner, C. A., Loffing-Cueni, D., Yan, Q., Schulz, N., Fakitsas, P., Carrel, M., Wang, T., Verrey, F., Geibel, J. P., Giebisch, G., Hebert, S. C., & Loffing, J. (2008). Mouse model of type II Bartter’s syndrome. II. Altered expression of renal sodium- and water-transporting proteins. American Journal of Physiology : Renal Physiology, 294(6), 1373–1380. https://doi.org/10.1152/ajprenal.00613.2007
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Bartter's syndrome represents a group of hereditary salt- and water-losing renal tubulopathies caused by loss-of-function mutations in proteins mediating or regulating salt transport in the thick ascending limb (TAL) of Henle's loop. Mutations in the ROMK channel cause type II antenatal Bartter's syndrome that presents with maternal polyhydramnios and postnatal life-threatening volume depletion. We have developed a colony of Romk null mice showing a Bartter-like phenotype and with increased survival to adulthood, suggesting the activa
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Wagner, C. A., Loffing-Cueni, D., Yan, Q., Schulz, N., Fakitsas, P., Carrel, M., Wang, T., Verrey, F., Geibel, J. P., Giebisch, G., Hebert, S. C., & Loffing, J. (2008). Mouse model of type II Bartter’s syndrome. II. Altered expression of renal sodium- and water-transporting proteins. American Journal of Physiology : Renal Physiology, 294(6), 1373–1380. https://doi.org/10.1152/ajprenal.00613.2007