Oleh Pochynyuk

Ras couples phosphoinositide 3-OH kinase to the epithelial Na+ channel.

Identification of a functional phosphatidylinositol 3,4,5-trisphosphate binding site in the epithelial Na+ channel.

Regulation of epithelial Na+ channel activity by conserved serine/threonine switches within sorting signals.

Regulation of the epithelial Na+ channel (ENaC) by phosphatidylinositides.

Rapid translocation and insertion of the epithelial Na+ channel in response to RhoA signaling.

Functional reconstitution of the human epithelial Na+ channel in a mammalian expression system.

Binding and direct activation of the epithelial Na+ channel (ENaC) by phosphatidylinositides.

Quantifying RhoA facilitated trafficking of the epithelial Na+ channel toward the plasma membrane with total internal reflection fluorescence-fluorescence recovery after photobleaching.

Acute regulation of the epithelial Na+ channel by phosphatidylinositide 3-OH kinase signaling in native collecting duct principal cells.

Molecular determinants of PI(4,5)P2 and PI(3,4,5)P3 regulation of the epithelial Na+ channel.

Purinergic control of apical plasma membrane PI(4,5)P2 levels sets ENaC activity in principal cells.

Ion channel regulation by Ras, Rho, and Rab small GTPases.

Insight toward epithelial Na+ channel mechanism revealed by the acid-sensing ion channel 1 structure.

Regulation of the epithelial Na+ channel by endothelin-1 in rat collecting duct.

Physiologic regulation of the epithelial sodium channel by phosphatidylinositides.

Paracrine regulation of the epithelial Na+ channel in the mammalian collecting duct by purinergic P2Y2 receptor tone.

Thiazolidinedione-induced fluid retention is independent of collecting duct alphaENaC activity.

Intrinsic voltage dependence of the epithelial Na+ channel is masked by a conserved transmembrane domain tryptophan.

Activation of the epithelial Na+ channel in the collecting duct by vasopressin contributes to water reabsorption.

Dietary Na+ inhibits the open probability of the epithelial sodium channel in the kidney by enhancing apical P2Y2-receptor tone.

Endothelin-1 inhibits the epithelial Na+ channel through betaPix/14-3-3/Nedd4-2.

Purinergic inhibition of ENaC produces aldosterone escape.

Acute cholesterol-induced anti-natriuretic effects: role of epithelial Na+ channel activity, protein levels, and processing.

Bradykinin acutely inhibits activity of the epithelial Na+ channel in mammalian aldosterone-sensitive distal nephron.

Voltage-dependent gating underlies loss of ENaC function in Pseudohypoaldosteronism type 1.

Af17 deficiency increases sodium excretion and decreases blood pressure.

Purinergic activation of Ca2+-permeable TRPV4 channels is essential for mechano-sensitivity in the aldosterone-sensitive distal nephron.

Role of collecting duct AT1a receptors in concentrating urine.

Angiotensin II increases activity of the epithelial Na+ channel (ENaC) in distal nephron additively to aldosterone.

Function of transient receptor potential cation channel subfamily V member 4 (TRPV4) as a mechanical transducer in flow-sensitive segments of renal collecting duct system.

Salt-dependent inhibition of epithelial Na+ channel-mediated sodium reabsorption in the aldosterone-sensitive distal nephron by bradykinin.

Direct activation of ENaC by angiotensin II: recent advances and new insights.

Novel insights into TRPV4 function in the kidney.

TRPV4 dysfunction promotes renal cystogenesis in autosomal recessive polycystic kidney disease.

Primary aldosteronism and impaired natriuresis in mice underexpressing TGFβ1.

Recording ion channels in isolated, split-opened tubules.

Ca2+ Imaging as a tool to assess TRP channel function in murine distal nephrons.

Discrete control of TRPV4 channel function in the distal nephron by protein kinases A and C.

Direct inhibition of basolateral Kir4.1/5.1 and Kir4.1 channels in the cortical collecting duct by dopamine.

Chronic angiotensin II infusion drives extensive aldosterone-independent epithelial Na+ channel activation.

Direct regulation of ENaC by bradykinin in the distal nephron. Implications for renal sodium handling.

Emerging role of the calcium-activated, small conductance, SK3 K+ channel in distal tubule function: regulation by TRPV4.

IGF-1 and insulin exert opposite actions on ClC-K2 activity in the cortical collecting ducts.

Control of ENaC-mediated sodium reabsorption in the distal nephron by Bradykinin.