Christoph Korbmacher

Sensitisation of TRPV4 by PAR2 is independent of intracellular calcium signalling and can be mediated by the biased agonist neutrophil elastase.

Basolateral PAR-2 receptors mediate KCl secretion and inhibition of Na+ absorption in the mouse distal colon.

Intrinsic sensitivity of Kir1.1 (ROMK) to glibenclamide in the absence of SUR2B. Implications for the identity of the renal ATP-regulated secretory K+ channel.

Cystic fibrosis transmembrane conductance regulator-dependent up-regulation of Kir1.1 (ROMK) renal K+ channels by the epithelial sodium channel.

Regulation of the epithelial sodium channel by N4WBP5A, a novel Nedd4/Nedd4-2-interacting protein.

The role of individual Nedd4-2 (KIAA0439) WW domains in binding and regulating epithelial sodium channels.

The serum and glucocorticoid-inducible kinase SGK1 and the Na+/H+ exchange regulating factor NHERF2 synergize to stimulate the renal outer medullary K+ channel ROMK1.

Identification of domains that control the heteromeric assembly of Kir5.1/Kir4.0 potassium channels.

Basolateral adrenoceptor activation mediates noradrenaline-induced Cl- secretion in M-1 mouse cortical collecting duct cells.

The gamma-subunit of ENaC is more important for channel surface expression than the beta-subunit.

cAMP-dependent activation of CFTR inhibits the epithelial sodium channel (ENaC) without affecting its surface expression.

Extracellular Na+ removal attenuates rundown of the epithelial Na+-channel (ENaC) by reducing the rate of channel retrieval.

Additional disruption of the ClC-2 Cl(-) channel does not exacerbate the cystic fibrosis phenotype of cystic fibrosis transmembrane conductance regulator mouse models.

PGE2 stimulates Cl- secretion in murine M-1 cortical collecting duct cells in an autocrine manner.

A novel pathway of epithelial sodium channel activation involves a serum- and glucocorticoid-inducible kinase consensus motif in the C terminus of the channel's alpha-subunit.

Stimulation of the epithelial sodium channel (ENaC) by the serum- and glucocorticoid-inducible kinase (Sgk) involves the PY motifs of the channel but is independent of sodium feedback inhibition.

Stimulation of the epithelial sodium channel (ENaC) by cAMP involves putative ERK phosphorylation sites in the C termini of the channel's beta- and gamma-subunit.

Functional characterization of a novel CFTR mutation P67S identified in a patient with atypical cystic fibrosis.

(NDRG2) stimulates amiloride-sensitive Na+ currents in Xenopus laevis oocytes and fisher rat thyroid cells.

Aldosterone responsiveness of the epithelial sodium channel (ENaC) in colon is increased in a mouse model for Liddle's syndrome.

Trypsin can activate the epithelial sodium channel (ENaC) in microdissected mouse distal nephron.

Cleavage in the {gamma}-subunit of the epithelial sodium channel (ENaC) plays an important role in the proteolytic activation of near-silent channels.

Plasmin in nephrotic urine activates the epithelial sodium channel.

Regulated sodium transport in the renal connecting tubule (CNT) via the epithelial sodium channel (ENaC).

HIF-prolyl hydroxylases in the rat kidney: physiologic expression patterns and regulation in acute kidney injury.

Mutations in the amiloride-sensitive epithelial sodium channel in patients with cystic fibrosis-like disease.

The delta-subunit of the epithelial sodium channel (ENaC) enhances channel activity and alters proteolytic ENaC activation.

Cholesterol depletion of the plasma membrane prevents activation of the epithelial sodium channel (ENaC) by SGK1.

Functional characterization of a partial loss-of-function mutation of the epithelial sodium channel (ENaC) associated with atypical cystic fibrosis.

A mutation of the epithelial sodium channel associated with atypical cystic fibrosis increases channel open probability and reduces Na+ self inhibition.

Proteolytic activation of the epithelial sodium channel (ENaC) in health and disease.

Protein kinase B alpha (PKBα) stimulates the epithelial sodium channel (ENaC) heterologously expressed in Xenopus laevis oocytes by two distinct mechanisms.

Atomic force microscopy reveals the architecture of the epithelial sodium channel (ENaC).

Four subunits (αβγδ) of the epithelial sodium channel (ENaC) are expressed in the human eye in various locations.

An inhibitory peptide derived from the α-subunit of the epithelial sodium channel (ENaC) shows a helical conformation.

Proteolytic activation of the epithelial sodium channel (ENaC) by the cysteine protease cathepsin-S.

Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron.

Plasmin and chymotrypsin have distinct preferences for channel activating cleavage sites in the γ subunit of the human epithelial sodium channel.

A mutation in the β-subunit of ENaC identified in a patient with cystic fibrosis-like symptoms has a gain-of-function effect.

Characterization of the mouse ClC-K1/Barttin chloride channel.

The bile acid receptor TGR5 does not interact with β-arrestins or traffic to endosomes but transmits sustained signals from plasma membrane rafts.

Pharmacological and electrophysiological characterization of the human bile acid-sensitive ion channel (hBASIC).

Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites.