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1.
Bohnert, B.N. et al.: Experimental nephrotic syndrome leads to proteolytic activation of the epithelial sodium channel (ENaC) in the mouse kidney. Am. J. Physiol.-Renal Physiol. 321, F480-F493 (2021)
2.
Fischereder, M.* et al.: Sodium storage in human tissues is mediated by glycosaminoglycan expression. Am. J. Physiol.-Renal Physiol. 313, F319-F325 (2017)
3.
Mulay, S.R.* et al.: Oxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice. Am. J. Physiol.-Renal Physiol. 310, F785-F795 (2016)
4.
Kemter, E.* et al.: Mutation of the Na⁺-K⁺-2Cl‾ cotransporter NKCC2 in mice is associated with severe polyuria and a urea-selective concentrating defect without hyperreninemia. Am. J. Physiol.-Renal Physiol. 298, F1405-F1415 (2010)
5.
Kemter, E.* et al.: Novel missense mutation of uromodulin in mice causes renal dysfunction with alterations in urea handling, energy, and bone metabolism. Am. J. Physiol.-Renal Physiol. 297, F1391-F1398 (2009)
6.
Aigner, B.* et al.: Screening for increased plasma urea levels in a large-scale ENU mouse mutagenesis project reveals kidney disease models. Am. J. Physiol.-Renal Physiol. 292, 1560-1567 (2007)