G Seebohm

Summary

Country: Germany

Publications

  1. pmc Position of aromatic residues in the S6 domain, not inactivation, dictates cisapride sensitivity of HERG and eag potassium channels
    Jun 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
  2. doi request reprint Altered stress stimulation of inward rectifier potassium channels in Andersen-Tawil syndrome
    Guiscard Seebohm
    Department of Biochemistry I Cation Channel Group, Ruhr University Bochum, Bochum, Germany
    FASEB J 26:513-22. 2012
  3. doi request reprint Long QT syndrome-associated mutations in KCNQ1 and KCNE1 subunits disrupt normal endosomal recycling of IKs channels
    Guiscard Seebohm
    Department of Physiology I, University of Tuebingen, Germany
    Circ Res 103:1451-7. 2008
  4. ncbi request reprint Regulation of endocytic recycling of KCNQ1/KCNE1 potassium channels
    Guiscard Seebohm
    Department of Physiology I, University of Tuebingen, Gmelinstrasse 5, D 72076 Tuebingen, Germany
    Circ Res 100:686-92. 2007
  5. pmc Differential roles of S6 domain hinges in the gating of KCNQ potassium channels
    Guiscard Seebohm
    Physiologisches Institut I, Universitat Tubingen, D 72076 Tubingen, Germany
    Biophys J 90:2235-44. 2006
  6. pmc Mutation of colocalized residues of the pore helix and transmembrane segments S5 and S6 disrupt deactivation and modify inactivation of KCNQ1 K+ channels
    Guiscard Seebohm
    Department of Physiology I, Universität Tuebingen, Gmelinstr 5, D 72076 Tuebingen, Germany
    J Physiol 563:359-68. 2005
  7. ncbi request reprint Activators of cation channels: potential in treatment of channelopathies
    Guiscard Seebohm
    Physiologisches Institut 1, Universität Tuebingen, Gmelinstr 5, D 72076 Tuebingen, Germany
    Mol Pharmacol 67:585-8. 2005
  8. ncbi request reprint Dependence of I(Ks) biophysical properties on the expression system
    G Seebohm
    Aventis Pharma Deutschland, Frankfurt M, Germany
    Pflugers Arch 442:891-5. 2001
  9. doi request reprint Long QT syndrome-associated mutations in the voltage sensor of I(Ks) channels
    Ulrike Henrion
    Department of Physiology I, University of Tuebingen, Tuebingen, Germany
    Cell Physiol Biochem 24:11-6. 2009
  10. pmc A kinetic study on the stereospecific inhibition of KCNQ1 and I(Ks) by the chromanol 293B
    G Seebohm
    Aventis Pharma Deutschland GmbH, DG Cardiovascular Diseases, D 65926 Frankfurt am Main, Germany
    Br J Pharmacol 134:1647-54. 2001

Collaborators

Detail Information

Publications44

  1. pmc Position of aromatic residues in the S6 domain, not inactivation, dictates cisapride sensitivity of HERG and eag potassium channels
    Jun 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...
  2. doi request reprint Altered stress stimulation of inward rectifier potassium channels in Andersen-Tawil syndrome
    Guiscard 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...
  3. doi request reprint Long QT syndrome-associated mutations in KCNQ1 and KCNE1 subunits disrupt normal endosomal recycling of IKs channels
    Guiscard 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...
  4. ncbi request reprint Regulation of endocytic recycling of KCNQ1/KCNE1 potassium channels
    Guiscard Seebohm
    Department of Physiology I, University of Tuebingen, Gmelinstrasse 5, D 72076 Tuebingen, Germany
    Circ Res 100:686-92. 2007
    ....
  5. pmc Differential roles of S6 domain hinges in the gating of KCNQ potassium channels
    Guiscard Seebohm
    Physiologisches Institut I, Universitat Tubingen, D 72076 Tubingen, Germany
    Biophys J 90:2235-44. 2006
    ....
  6. pmc Mutation of colocalized residues of the pore helix and transmembrane segments S5 and S6 disrupt deactivation and modify inactivation of KCNQ1 K+ channels
    Guiscard 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...
  7. ncbi request reprint Activators of cation channels: potential in treatment of channelopathies
    Guiscard Seebohm
    Physiologisches Institut 1, Universität Tuebingen, Gmelinstr 5, D 72076 Tuebingen, Germany
    Mol Pharmacol 67:585-8. 2005
    ....
  8. ncbi request reprint Dependence of I(Ks) biophysical properties on the expression system
    G 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...
  9. doi request reprint Long QT syndrome-associated mutations in the voltage sensor of I(Ks) channels
    Ulrike 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...
  10. pmc A kinetic study on the stereospecific inhibition of KCNQ1 and I(Ks) by the chromanol 293B
    G 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...
  11. ncbi request reprint Functional coassembly of KCNQ4 with KCNE-beta- subunits in Xenopus oocytes
    Nathalie 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...
  12. pmc Tight coupling of rubidium conductance and inactivation in human KCNQ1 potassium channels
    Guiscard Seebohm
    Department of Physiology, University of Utah, Salt Lake City, UT USA, Physiologisches Institut I, Tubingen, Germany
    J Physiol 552:369-78. 2003
    ....
  13. ncbi request reprint Functional significance of the kainate receptor GluR6(M836I) mutation that is linked to autism
    Nathalie 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)...
  14. doi request reprint Novel insights into the structural basis of pH-sensitivity in inward rectifier K+ channels Kir2.3
    Oana 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...
  15. doi request reprint Differential modulation of cardiac potassium channels by Grb adaptor proteins
    Oana 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...
  16. doi request reprint Regulation of the glutamate transporter EAAT2 by PIKfyve
    Eva 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...
  17. ncbi request reprint Modulation of human Kv1.5 channel kinetics by N-cadherin
    Evgenia 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...
  18. ncbi request reprint Regulation of cardiac shal-related potassium channel Kv 4.3 by serum- and glucocorticoid-inducible kinase isoforms in Xenopus oocytes
    Ravshan 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...
  19. ncbi request reprint Regulation of KCNQ4 potassium channel prepulse dependence and current amplitude by SGK1 in Xenopus oocytes
    Guiscard 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...
  20. ncbi request reprint Additive regulation of GluR1 by stargazin and serum- and glucocorticoid-inducible kinase isoform SGK3
    Nathalie 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...
  21. doi request reprint PIKfyve-dependent regulation of the Cl- channel ClC-2
    Fabian 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...
  22. ncbi request reprint Regulation of the Na(+)-coupled glutamate transporter EAAT3 by PIKfyve
    Fabian 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...
  23. doi request reprint PIP5K2A-dependent regulation of excitatory amino acid transporter EAAT3
    Olga 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...
  24. doi request reprint PIKfyve upregulates CFTR activity
    Eva 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...
  25. doi request reprint Regulation of the glutamate transporter EAAT4 by PIKfyve
    Ioana 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...
  26. doi request reprint A schizophrenia-linked mutation in PIP5K2A fails to activate neuronal M channels
    Olga 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...
  27. ncbi request reprint Regulation of the Na(+), glucose cotransporter by PIKfyve and the serum and glucocorticoid inducible kinase SGK1
    Manzar 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...
  28. pmc Glucocorticoid adrenal steroids and glucocorticoid-inducible kinase isoforms in the regulation of GluR6 expression
    Nathalie 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...
  29. ncbi request reprint Influence of gain of function epithelial chloride channel ClC-Kb mutation on hearing thresholds
    Andreas Frey
    Department of Physiology, University of Tubingen, Gmelinstrasse 5, D 72076 Tubingen, 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...
  30. pmc Regulation of GluR1 abundance in murine hippocampal neurones by serum- and glucocorticoid-inducible kinase 3
    Nathalie 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...
  31. ncbi request reprint Chromanol 293B binding in KCNQ1 (Kv7.1) channels involves electrostatic interactions with a potassium ion in the selectivity filter
    Christian Lerche
    Physiology I, University of Tuebingen, Tuebingen, Germany
    Mol Pharmacol 71:1503-11. 2007
    ....
  32. ncbi request reprint Comparison of potent Kv1.5 potassium channel inhibitors reveals the molecular basis for blocking kinetics and binding mode
    Nathalie 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...
  33. ncbi request reprint Association of the serum and glucocorticoid regulated kinase (sgk1) gene with QT interval
    Andreas Busjahn
    Franz Volhard Clinic, HELIOS Kliniken Berlin and Max Delbrück Center for Molecular Medicine, Medical Faculty of the Charite, 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...
  34. ncbi request reprint Molecular determinants of KCNQ1 channel block by a benzodiazepine
    Guiscard Seebohm
    Department of Physiology, University of Utah, Salt Lake City, USA
    Mol Pharmacol 64:70-7. 2003
    ....
  35. ncbi request reprint The new anticonvulsant retigabine favors voltage-dependent opening of the Kv7.2 (KCNQ2) channel by binding to its activation gate
    Thomas V Wuttke
    Neurologische Klinik Abteilung Angewandte Physiologie, Universitat Ulm, 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...
  36. ncbi request reprint Pharmacological activation of normal and arrhythmia-associated mutant KCNQ1 potassium channels
    Guiscard 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...
  37. ncbi request reprint Functional analysis of Caenorhabditis elegans glutamate receptor subunits by domain transplantation
    Nathalie 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...
  38. pmc C-terminal interaction of KCNQ2 and KCNQ3 K+ channels
    Snezana 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...
  39. ncbi request reprint PIKfyve in the SGK1 mediated regulation of the creatine transporter SLC6A8
    Nathalie 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)...
  40. ncbi request reprint Alterations in the cytoplasmic domain of CLCN2 result in altered gating kinetics
    Jochen 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...
  41. pmc An inactivation gate in the selectivity filter of KCNQ1 potassium channels
    Gilad 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...
  42. ncbi request reprint Serum- and glucocorticoid-inducible kinase 1 (SGK1) mediates glucocorticoid-induced inhibition of insulin secretion
    Susanne 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...
  43. pmc GLUT1 mutations are a cause of paroxysmal exertion-induced dyskinesias and induce hemolytic anemia by a cation leak
    Yvonne G Weber
    Neurologische Klinik and Institut für Anatomie und Zellbiologie, Universitat Ulm, Ulm, Germany
    J Clin Invest 118:2157-68. 2008
    ....
  44. pmc Neutralization of a negative charge in the S1-S2 region of the KV7.2 (KCNQ2) channel affects voltage-dependent activation in neonatal epilepsy
    Thomas 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...