Daria V. Ilatovskaya

Intact cytoskeleton is required for small G protein dependent activation of the epithelial Na+ channel.

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

The actin cytoskeleton and small G protein RhoA are not involved in flow-dependent activation of ENaC.

Novel role of Rac1/WAVE signaling mechanism in regulation of the epithelial Na+ channel.

NSAIDs acutely inhibit TRPC channels in freshly isolated rat glomeruli.

Cortical actin binding protein cortactin mediates ENaC activity via Arp2/3 complex.

Effects of cytochrome P-450 metabolites of arachidonic acid on the epithelial sodium channel (ENaC).

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

ROS production as a common mechanism of ENaC regulation by EGF, insulin, and IGF-1.

G-protein signaling modulator 1 deficiency accelerates cystic disease in an orthologous mouse model of autosomal dominant polycystic kidney disease.

Single-channel analysis of TRPC channels in the podocytes of freshly isolated Glomeruli.

Regulation of ENaC in mice lacking renal insulin receptors in the collecting duct.

Real-time electrochemical detection of ATP and H₂O₂ release in freshly isolated kidneys.

Deficiency of renal cortical EGF increases ENaC activity and contributes to salt-sensitive hypertension.

Epidermal growth factors in the kidney and relationship to hypertension.

Arp2/3 complex inhibitors adversely affect actin cytoskeleton remodeling in the cultured murine kidney collecting duct M-1 cells.

Pharmacological characterization of the P2 receptors profile in the podocytes of the freshly isolated rat glomeruli.

Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli.

Impaired epithelial Na+ channel activity contributes to cystogenesis and development of autosomal recessive polycystic kidney disease in PCK rats.

Cross-talk between insulin and IGF-1 receptors in the cortical collecting duct principal cells: implication for ENaC-mediated Na+ reabsorption.

TRPC6 channel as an emerging determinant of the podocyte injury susceptibility in kidney diseases.