Hauptinhalt

Auswahl von Originalpublikationen der letzten fünf Jahre:

  • Grgic I, Kiss E, Kaistha BP, Busch C, kloss M, Sautter J, Müller A., Kaistha A, Schmidt C, Raman G, Wulff H, Strutz F, Gröne H-J, Köhler R, Hoyer J. Renal fibrosis is attenuated by targeted disruption of Kca3.1 potassium channels. Proc Natl Acad Sci USA 106: 14518-23, 2009. [IF: 9.4]

  • Brähler S, Kaistha A, Schmidt J, Wölfle SE, Busch C, Kaistha BP, Kacik M, Hasenau AL, Grgic I, Si H, Bond CT, Adelman JP, Wulff H, deWit C, Hoyer J, Köhler R. Genetic defizit of SK3 and IK1 channels disrupts the endothelium-derived hyperpolarizing factor vasodilator pathway and causes hypertension. Circulation 119: 2323-32, 2009. [IF: 14.6]

  • Grgic I, Si H, Depboylu C, Höglinger GU, Busch C, Heyken WT, Kuhlmann U, Maier T, Köhler R, Hoyer J. Hyperkalaemia in a tetraplegic adolescent due to de novo sodium channel mutation. Nephrol Dial Transplant. 23: 1449-51, 2008. [IF: 3.2]

  • Hartmannsgruber V, Heyken WT, Kacik M, Kaistha A, Grgic I, Harteneck C, Liedtke W, Hoyer J, Kohler R. Arterial response to shear stress critically depends on endothelial TRPV4 expression. PLoS ONE. 2007 Sep 5; 2(9):e827. [IF: not determined]

  • Si H, Heyken WT, Wolfle SE, Tysiac M, Schubert R, Grgic I, Vilianovich L, Giebing G, Maier T, Gross V, Bader M, de Wit C, Hoyer J, Köhler R. Impaired endothelium-derived hyperpolarizing factor-mediated dilations and increased blood pressure in mice deficient of the intermediate-conductance Ca2+-activated K+ channel. Circ Res 99: 537-544, 2006. [IF: 9.9]

  • Si H, Grgic I, Heyken WT, Maier T, Hoyer J, Reusch HP, Köhler R. Mitogenic modulation of Ca2+-activated K+ channels in proliferating A7r5 vascular smooth muscle cells. Br J Pharmacol 148(7):909-17, 2006. [IF: 3.8]

  • Köhler R, Heyken WT, Heinau P, Schubert R, Si H, Kacik M, Busch C, Grgic I, Maier T, Hoyer J. Evidence for a functional role of endothelial transient receptor potential V4 in shear stress-induced vasodilatation. Arterioscler Thromb Vasc Biol 26:1495-502, 2006. [IF: 6.9]

  • Köhler R, Eichler I, Schönfelder H, Grgic I, Heinau P, Si H, Hoyer J. Impaired EDHF-mediated vasodilation and function of endothelial Ca2+-activated K+ channels in uremic rats. Kidney Int 67: 2280-7, 2005. [IF: 4.8]

  • Grgic I, Eichler I, Heinau P, Si H, Brakemeier S, Hoyer J, Köhler R. Selective Blockade of the intermediate-conductance Ca2+-activated K+ channel suppresses proliferation of microvascular and macrovascular endothelial cells and angiogenesis in vivo. Arterioscler Thromb Vasc Biol 25: 704-9, 2005. [IF: 6.9]

  • Köhler R, Eichler I, Schönfelder H, Grgic I, Heinau P, Si H, Hoyer J. Impaired EDHF-mediated vasodilation and function of endothelial Ca2+-activated K+ channels in uremic rats. Kidney Int 67: 2280-7, 2005. [IF: 4.8]

  • Maier T, Grgic I, Busch C, Hoyer J, Kohler R. Endothelial ion channels - novel targets for antihypertensive therapy. Dtsch Med Wochenschr. 130:2637-9, 2005. [IF: 0.4]

  • Grgic I, Eichler I, Heinau P, Si H, Brakemeier S, Hoyer J, Kohler R. Selective blockade of the intermediate-conductance Ca2+-activated K+ channel suppresses proliferation of microvascular and macrovascular endothelial cells and angiogenesis in vivo. Arterioscler Thromb Vasc Biol. 25: 704-709, 2005. [IF: 7.4]

  • Brakemeier S, Si H, Gollasch M, Höffler D, Buhl B, Köhler R, Hoyer J, Eichler I. Dent's disease: Identification of a novel mutation in the renal chloride channel CLCN5. Clin Nephrol 62:387-90, 2004. [IF: 1.4]

  • Brakemeier S, Eichler I, Knorr A, Fassheber T, Köhler R, Hoyer J.. Modulation of Ca2+-activated K+ channel in renal artery endothelium in situ by NO and reactive oxygen species. Kidney Int. 64: 199-207, 2003. [IF: 4.8]

  • Köhler R, Wulff H, Eichler I, Kneifel M, Neumann D, Knorr A, Grgic I, Kämpfe D, Brakemeier S, Orzechowski HD, Reusch HP, Paul M, Chandy KG, Hoyer J..Blockade of the IKCa1 Ca2+-activated K+ channel as a new therapeutic strategy for restenosis. Circulation, 108: 1119-25, 2003. [IF:14.6]