Research Topics
Species | G SeebohmSummaryCountry: Germany Publications
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Publications
Position of aromatic residues in the S6 domain, not inactivation, dictates cisapride sensitivity of HERG and eag potassium channelsJun Chen
Department of Internal Medicine, University of Utah, 15 North 2030 East, Room 4220, Salt Lake City, UT 84112, USA
Proc Natl Acad Sci U S A 99:12461-6. 2002..These findings suggest that positioning of S6 aromatic residues relative to the central cavity of the channel, not inactivation per se determines drug block of HERG or eag channels...- Altered stress stimulation of inward rectifier potassium channels in Andersen-Tawil syndromeGuiscard Seebohm
Department of Biochemistry I Cation Channel Group, Ruhr University Bochum, Bochum, Germany
FASEB J 26:513-22. 2012..1 genotype. Thus, our findings provide a possible explanation for the contradictory effects of glucocorticoid treatment on symptoms in patients with ATS and may open new pathways for the design of personalized medicines in ATS therapy... - Long QT syndrome-associated mutations in KCNQ1 and KCNE1 subunits disrupt normal endosomal recycling of IKs channelsGuiscard Seebohm
Department of Physiology I, University of Tuebingen, Germany
Circ Res 103:1451-7. 2008..Identification of the I(Ks) recycling pathway and its modulation by stress-stimulated SGK1 provides novel mechanistic insight into potentially fatal cardiac arrhythmias triggered by physical or psychological stress... - Regulation of endocytic recycling of KCNQ1/KCNE1 potassium channelsGuiscard Seebohm
Department of Physiology I, University of Tuebingen, Gmelinstrasse 5, D 72076 Tuebingen, Germany
Circ Res 100:686-92. 2007.... - Differential roles of S6 domain hinges in the gating of KCNQ potassium channelsGuiscard Seebohm
Physiologisches Institut I, Universitat Tubingen, D 72076 Tubingen, Germany
Biophys J 90:2235-44. 2006.... - Mutation of colocalized residues of the pore helix and transmembrane segments S5 and S6 disrupt deactivation and modify inactivation of KCNQ1 K+ channelsGuiscard Seebohm
Department of Physiology I, Universität Tuebingen, Gmelinstr 5, D 72076 Tuebingen, Germany
J Physiol 563:359-68. 2005..Disturbance of these interactions might underly LQTS associated with KCNQ1 mutant channels... - Activators of cation channels: potential in treatment of channelopathiesGuiscard Seebohm
Physiologisches Institut 1, Universität Tuebingen, Gmelinstr 5, D 72076 Tuebingen, Germany
Mol Pharmacol 67:585-8. 2005.... - Dependence of I(Ks) biophysical properties on the expression systemG Seebohm
Aventis Pharma Deutschland, Frankfurt M, Germany
Pflugers Arch 442:891-5. 2001..The sensitivity to the extracellular potassium concentration, temperature dependency and kinetics differ qualitatively. Potentially there is an endogenous component that affects I(Ks) which does not appear in all expression systems... - Long QT syndrome-associated mutations in the voltage sensor of I(Ks) channelsUlrike Henrion
Department of Physiology I, University of Tuebingen, Tuebingen, Germany
Cell Physiol Biochem 24:11-6. 2009..All three mutations reduced KCNQ1/KCNE1 channel currents in a dominant-negative manner when the mutants were coexpressed with wt subunits suggesting reduced I(Ks) as the molecular basis of LQT1... - A kinetic study on the stereospecific inhibition of KCNQ1 and I(Ks) by the chromanol 293BG Seebohm
Aventis Pharma Deutschland GmbH, DG Cardiovascular Diseases, D 65926 Frankfurt am Main, Germany
Br J Pharmacol 134:1647-54. 2001..e. positive use-dependency. This enantiomer therefore represents a valuable pharmacological tool to evaluate the therapeutic efficiency of I(Ks)blockade... - Functional coassembly of KCNQ4 with KCNE-beta- subunits in Xenopus oocytesNathalie Strutz Seebohm
Department of Physiology, University of Tuebingen, Tuebingen, Germany
Cell Physiol Biochem 18:57-66. 2006..In conclusion, KCNEs are presumably coexpressed with KCNQ4 in hair cells from the organ of Corti and might regulate KCNQ4 functional properties, effects that could be important under physiological and pathophysiological conditions... - Tight coupling of rubidium conductance and inactivation in human KCNQ1 potassium channelsGuiscard Seebohm
Department of Physiology, University of Utah, Salt Lake City, UT USA, Physiologisches Institut I, , Germany
J Physiol 552:369-78. 2003.... - Functional significance of the kainate receptor GluR6(M836I) mutation that is linked to autismNathalie Strutz-Seebohm
Department of Physiology I, University of Tuebingen, Tuebingen, Germany
Cell Physiol Biochem 18:287-94. 2006..Furthermore, we identified new mechanisms determining the plasma membrane abundance of wild type GluR6 and GluR6(M836I)... - Novel insights into the structural basis of pH-sensitivity in inward rectifier K+ channels Kir2.3Oana N Ureche
Physiology I, University of Tuebingen, Germany
Cell Physiol Biochem 21:347-56. 2008..The data provide molecular insight into the unique pH regulation of inward rectifier channels... - Differential modulation of cardiac potassium channels by Grb adaptor proteinsOana N Ureche
Physiologisches Institut 1, University Tuebingen, Tuebingen, Germany
Biochem Biophys Res Commun 384:28-31. 2009..1 and Kir2.2 channels. The present observations for the first time provide evidence for a selective and modulatory role of Grb adaptor proteins in the functional expression of cardiac K(+) channels... - Regulation of the glutamate transporter EAAT2 by PIKfyveEva Maria Gehring
Department of Physiology I, University of Tubingen, Germany
Cell Physiol Biochem 24:361-8. 2009..Confocal microscopy reveals that PIKfyve enhances the EAAT2 protein abundance in the cell membrane. The observations disclose that PIKfyve indeed participates in the regulation of EAAT2... - Modulation of human Kv1.5 channel kinetics by N-cadherinEvgenia Koutsouki
Department of Physiology, University of Tubingen, Gmelinstr 5, D 72076 Tubingen, Germany
Biochem Biophys Res Commun 363:18-23. 2007..In conclusion, N-cadherin modifies Kv1.5 channel activity and is thus a novel candidate signaling molecule participating in the regulation of a variety of functions including cardiac action potential and vascular tone... - Regulation of cardiac shal-related potassium channel Kv 4.3 by serum- and glucocorticoid-inducible kinase isoforms in Xenopus oocytesRavshan Baltaev
Department of Physiology I, University of Tubingen, Tubingen, Germany
Pflugers Arch 450:26-33. 2005..2 or RAB5, nor did it reflect increased cell surface expression. In conclusion, SGK1 stimulates Kv 4.3 potassium channels expressed in Xenopus oocytes by a novel mechanism distinct from the known NEDD4.2-dependent pathway... - Regulation of KCNQ4 potassium channel prepulse dependence and current amplitude by SGK1 in Xenopus oocytesGuiscard Seebohm
Department of Physiology, University of Tuebingen, Germany
Cell Physiol Biochem 16:255-62. 2005..In conclusion, SGK1 regulates current amplitudes and kinetic properties of KCNQ4 channel activity, an effect sensitive to mutations in the SGK1 consensus sequence of the channel... - Additive regulation of GluR1 by stargazin and serum- and glucocorticoid-inducible kinase isoform SGK3Nathalie Strutz-Seebohm
Department of Physiology I, University of Tuebingen, 72076, Tuebingen, Germany
Pflugers Arch 452:276-82. 2006..In conclusion, SGK3 and stargazin regulate GluR1 independently, and thus, their effects on glutamate-induced currents are additive... - PIKfyve-dependent regulation of the Cl- channel ClC-2Fabian Klaus
Department of Physiology I, Physiologisches Institut I, University of Tubingen, Gmelinstr 5, D 72076 Tubingen, Germany
Biochem Biophys Res Commun 381:407-11. 2009..Coexpression of (S318A)PIKfyve significantly blunted the stimulating effect of (S422D)SGK1 on ClC-2-activity. In conclusion, PIKfyve is a potent stimulator of ClC-2-activity and contributes to SGK1-dependent regulation of ClC-2... - Regulation of the Na(+)-coupled glutamate transporter EAAT3 by PIKfyveFabian Klaus
Department of Physiology I, University of Tubingen, Germany
Neurochem Int 54:372-7. 2009..Moreover, additional coexpression of(S318A)PIKfyve significantly blunted I(glu) in Xenopus oocytes coexpressing SGK1 and EAAT3. The observations demonstrate that PIKfyve participates in EAAT3 regulation likely downstream of SGK1... - PIP5K2A-dependent regulation of excitatory amino acid transporter EAAT3Olga Fedorenko
Department of Physiology, University of Tuebingen, Gmelinstr 5, 72076 Tuebingen, Germany
Psychopharmacology (Berl) 206:429-35. 2009..A defect of the excitatory amino acid transporter EAAT3 has similarly been implicated in the development of schizophrenia. The present study thus explored whether PIP5K2A is involved in the regulation of EAAT3 activity... - PIKfyve upregulates CFTR activityEva Maria Gehring
Department of Physiology, University of Tubingen, Gmelinstrasse 5, D 72076 Tubingen, Germany
Biochem Biophys Res Commun 390:952-7. 2009..The present observations reveal a novel powerful regulator of intact but not of defective CFTR... - Regulation of the glutamate transporter EAAT4 by PIKfyveIoana S Alesutan
Department of Physiology I, University of Tubingen, D 72076 Tubingen, Germany
Cell Physiol Biochem 25:187-94. 2010..Furthermore, coexpression of (S318A)PIKfyve significantly blunted the stimulating effect of SGK1 on EAAT4 activity. The observations disclose that PIKfyve indeed participates in the regulation of EAAT4... - A schizophrenia-linked mutation in PIP5K2A fails to activate neuronal M channelsOlga Fedorenko
Department of Physiology, University of Tuebingen, Gmelinstr 5, 72076, Tuebingen, Germany
Psychopharmacology (Berl) 199:47-54. 2008..Activation of KCNQ accordingly attenuates the central stimulating effects of dopamine, cocaine, methylphenidate, and phenylcyclidine... - Regulation of the Na(+), glucose cotransporter by PIKfyve and the serum and glucocorticoid inducible kinase SGK1Manzar Shojaiefard
Department of Physiology I, University of Tubingen, Germany
Biochem Biophys Res Commun 359:843-7. 2007..Moreover, coexpression of (S138A)PIKfyve significantly blunted the effect of SGK1 on SLC5A1 activity. The observations disclose that PIKfyve participates in the SGK1-dependent regulation of SLC5A1... - Glucocorticoid adrenal steroids and glucocorticoid-inducible kinase isoforms in the regulation of GluR6 expressionNathalie Strutz-Seebohm
Department of Physiology I, University of Tuebingen, 72076 Tuebingen, Germany
J Physiol 565:391-401. 2005..The related kinases SGK2 and SGK3 similarly stimulate GluR6, but are less effective than SGK1. The observations point to a novel mechanism regulating GluR6 which contributes to the regulation of neuronal function by glucocorticoids... - Influence of gain of function epithelial chloride channel ClC-Kb mutation on hearing thresholdsAndreas Frey
Department of Physiology, , Gmelinstrasse 5, , Germany
Hear Res 214:68-75. 2006..In conclusion, hearing thresholds are slightly lower in carriers of ClC-Kb(T481S), i.e., the gain-of-function polymorphism ClC-Kb(T481S) exerts a subtle but significant protective effect against hearing loss... - Regulation of GluR1 abundance in murine hippocampal neurones by serum- and glucocorticoid-inducible kinase 3Nathalie Strutz-Seebohm
Department of Physiology I, University of Tuebingen, 72076 Tuebingen, Germany
J Physiol 565:381-90. 2005..The present observations disclose a novel mechanism in the regulation of GluR1... - Chromanol 293B binding in KCNQ1 (Kv7.1) channels involves electrostatic interactions with a potassium ion in the selectivity filterChristian Lerche
Physiology I, University of Tuebingen, Tuebingen, Germany
Mol Pharmacol 71:1503-11. 2007.... - Comparison of potent Kv1.5 potassium channel inhibitors reveals the molecular basis for blocking kinetics and binding modeNathalie Strutz Seebohm
Physiologisches Institut I, Universitat Tubingen, Tubingen, Germany
Cell Physiol Biochem 20:791-800. 2007..As S9947 and ICAGEN-4 show faster block with proceeding channel openings, formation of this tertiary complex may increasingly stabilise binding of S9947 and ICAGEN-4, thereby explaining open channel block kinetics of these compounds... - Association of the serum and glucocorticoid regulated kinase (sgk1) gene with QT intervalAndreas Busjahn
Franz Volhard Clinic, , Medical Faculty of the Charit, Humboldt University of Berlin, Germany
Cell Physiol Biochem 14:135-42. 2004..We conclude that the regulation of KCNE1/KCNQ1 by SGK1 is similarly relevant for the repolarization of cardiac myocytes as for regulation of renal ENaC activity and blood pressure control... - Molecular determinants of KCNQ1 channel block by a benzodiazepineGuiscard Seebohm
Department of Physiology, University of Utah, Salt Lake City, USA
Mol Pharmacol 64:70-7. 2003.... - The new anticonvulsant retigabine favors voltage-dependent opening of the Kv7.2 (KCNQ2) channel by binding to its activation gateThomas V Wuttke
Neurologische Klinik/Abteilung Angewandte Physiologie, , Zentrum Klinische Forschung, Helmholtzstrasse 8/1, 89081 Ulm, Germany
Mol Pharmacol 67:1009-17. 2005..We propose that RTG binds to a hydrophobic pocket formed upon channel opening between the cytoplasmic parts of S5 and S6 involving Trp236 and the channel's gate, which could well explain the strong shift in voltage-dependent activation... - Pharmacological activation of normal and arrhythmia-associated mutant KCNQ1 potassium channelsGuiscard Seebohm
Department of Physiology and Eccles Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah 84112, USA
Circ Res 93:941-7. 2003..Most KCNQ1 mutant channels responded to R-L3 similarly to wild-type channels, but one mutant channel (G306R) was insensitive to R-L3 possibly because it disrupted a key component of the drug-binding site... - Functional analysis of Caenorhabditis elegans glutamate receptor subunits by domain transplantationNathalie Strutz-Seebohm
Department of Biochemistry I, Receptor Biochemistry, Ruhr University Bochum, Bochum D-44780, Germany
J Biol Chem 278:44691-701. 2003..elegans can be occupied by other amino acids, including, surprisingly, lysine and proline, without loss of these properties... - C-terminal interaction of KCNQ2 and KCNQ3 K+ channelsSnezana Maljevic
Department of Applied Physiology, University of Ulm, Germany
J Physiol 548:353-60. 2003..Our results indicate that specific parts of the C-terminus enable the interaction between KCNQ2 and KCNQ3 channels and that different parts of the KCNQ3 C-terminus are important for regulating current amplitude... - PIKfyve in the SGK1 mediated regulation of the creatine transporter SLC6A8Nathalie Strutz-Seebohm
Department of Physiology I, University of Tubingen, Tubingen Germany
Cell Physiol Biochem 20:729-34. 2007..The observations suggest that SGK1 regulates the creatine transporter SLC6A8 at least partially through phosphorylation and activation of PIKfyve and subsequent formation of PI(3,5)P(2)... - Alterations in the cytoplasmic domain of CLCN2 result in altered gating kineticsJochen Paul
Department of Physiology, University of Tubingen, Germany
Cell Physiol Biochem 20:441-54. 2007..In conclusion, the Africans' gene pool comprises CLCN2 gene variants in the N-terminus, the C-terminus or the pore domain that affect surface expression and voltage- or cell-swelling-stimulated channel gating... - An inactivation gate in the selectivity filter of KCNQ1 potassium channelsGilad Gibor
Department of Physiology and Pharmacology, Sackler Medical School, Tel Aviv University, Tel Aviv, Israel
Biophys J 93:4159-72. 2007..We suggest that trapping of K(+) at s(1) due to filter rigidity and hindrance of the dehydration-resolvation transition underlie the slow inactivation of KCNQ1 pore mutants... - Serum- and glucocorticoid-inducible kinase 1 (SGK1) mediates glucocorticoid-induced inhibition of insulin secretionSusanne Ullrich
Department for Physiology, University of Tubingen, Tubingen, Germany
Diabetes 54:1090-9. 2005..Increased K(+) channel activity reduces Ca(2+) entry through voltage-gated Ca(2+) channels and insulin release... - GLUT1 mutations are a cause of paroxysmal exertion-induced dyskinesias and induce hemolytic anemia by a cation leakYvonne G Weber
Neurologische Klinik and Institut für Anatomie und Zellbiologie, Universitat Ulm, Ulm, Germany
J Clin Invest 118:2157-68. 2008.... - Neutralization of a negative charge in the S1-S2 region of the KV7.2 (KCNQ2) channel affects voltage-dependent activation in neonatal epilepsyThomas V Wuttke
Neurological Clinic, University of Ulm, Germany
J Physiol 586:545-55. 2008..On a molecular level, these results reveal a critical role in voltage sensing of the negatively charged E119 in S1-S2 of KV7.2, a region that-- according to molecular modelling - might interact with a positive charge in the S4 segment...