The ClC-5 chloride channel knock-out mouse – an animal model for Dent's disease Willy GüntherNils PiwonThomas J. Jentsch Mouse Models and Human Diseases Pages: 456 - 462
Inactivation of sodium-transporting proteins in the kidney I. Rubera B. Rossier E. Hummler Mouse Models and Human Diseases Pages: 463 - 469
Tubuloglomerular feedback in the kidney: insights from gene-targeted mice Volker Vallon Mouse Models and Human Diseases Pages: 470 - 476
Pathophysiological role of the mineralocorticoid receptor in heart: analysis of conditional transgenic models Antoine Ouvrard-PascaudFrédéric Jaisser Mouse Models and Human Diseases Pages: 477 - 481
A gene knockout approach in mice to identify glucose sensors controlling glucose homeostasis Bernard Thorens Mouse Models and Human Diseases Pages: 482 - 490
Current successes and limitations of using genetic modification for blood pressure research Linda MullinsJohn Mullins Mouse Models and Human Diseases Pages: 491 - 494
Regulation of airway surface liquid volume by human airway epithelia R. Boucher CFTR-ENaC Interactions Pages: 495 - 498
Functional interaction of CFTR and ENaC in sweat glands M. Reddy P. Quinton CFTR-ENaC Interactions Pages: 499 - 503
ENaC is inhibited by an increase in the intracellular Cl– concentration mediated through activation of Cl– channels Karl Kunzelmann CFTR-ENaC Interactions Pages: 504 - 512
cAMP-dependent activation of CFTR inhibits the epithelial sodium channel (ENaC) without affecting its surface expression Angelos-Aristeidis KonstasJan-Peter KochChristoph Korbmacher CFTR-ENaC Interactions Pages: 513 - 521
ENaC–CFTR interactions: the role of electrical coupling of ion fluxes explored in an epithelial cell model Jean-Daniel Horisberger CFTR-ENaC Interactions Pages: 522 - 528