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2. Unbiased kidney-centric molecular categorization of chronic kidney disease as a step towards precision medicine

Author

Reznichenko, Anna, Nair, Viji, Eddy, Sean, Fermin, Damian, Tomilo, Mark, Slidel, Timothy, Ju, Wenjun, Henry, Ian, Badal, Shawn S., Wesley, Johnna D., Liles, John T., Moosmang, Sven, Williams, Julie M., Quinn, Carol Moreno, Bitzer, Markus, Hodgin, Jeffrey B., Barisoni, Laura, Karihaloo, Anil, Breyer, Matthew D., Duffin, Kevin L., Patel, Uptal D., Magnone, Maria Chiara, Bhat, Ratan, and Kretzler, Matthias

Published
2024
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3. Differential In Vitro Effects of SGLT2 Inhibitors on Mitochondrial Oxidative Phosphorylation, Glucose Uptake and Cell Metabolism

Author

Zügner, Elmar, primary, Yang, Hsiu-Chiung, additional, Kotzbeck, Petra, additional, Boulgaropoulos, Beate, additional, Sourij, Harald, additional, Hagvall, Sepideh, additional, Elmore, Charles S., additional, Esterline, Russell, additional, Moosmang, Sven, additional, Oscarsson, Jan, additional, Pieber, Thomas R., additional, Peng, Xiao-Rong, additional, and Magnes, Christoph, additional

Published
2022
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5. Molecular Stratification of Chronic Kidney Disease

Author

Reznichenko, Anna, primary, Nair, Viji, additional, Eddy, Sean, additional, Tomilo, Mark, additional, Slidel, Timothy, additional, Ju, Wenjun, additional, Conway, James, additional, Badal, Shawn, additional, Wesley, Johnna, additional, Liles, John, additional, Moosmang, Sven, additional, Williams, Julie M, additional, Moreno Quinn, Carol, additional, Bitzer, Markus, additional, Karihaloo, Anil, additional, Breyer, Matthew, additional, Duffin, Kevin, additional, Patel, Uptal, additional, Magnone, Maria Chiara, additional, Bhat, Ratan, additional, and Kretzler, Matthias, additional

Published
2021
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7. Decreased cardiac L-type [Ca.sup.2+] channel activity induces hypertrophy and heart failure in mice

Author

Goonasekera, Sanjeewa A., Hammer, Karin, Auger-Messier, Mannix, Bodi, llona, Chen, Xiongwen, Zhang, Hongyu, Reiken, Steven, Elrod, John W., Correll, Robert N., York, Allen J., Sargent, Michelle A., Hofmann, Franz, Moosmang, Sven, Marks, Andrew R., Houser, Steven R., Bers, Donald M., and Molkentin, Jeffery D.

Subjects
Calcium channels -- Physiological aspects -- Research, Heart enlargement -- Diagnosis -- Risk factors -- Research -- Genetic aspects, Health care industry
Abstract

Antagonists of L-type [Ca.sup.2+] channels (LTCCs) have been used to treat human cardiovascular diseases for decades. However, these inhibitors can have untoward effects in patients with heart failure, and their overall therapeutic profile remains nebulous given differential effects in the vasculature when compared with those in cardiomyocytes. To investigate this issue, we examined mice heterozygous for the gene encoding the pore-forming subunit of LTCC (calcium channel, voltage-dependent, L type, α1C subunit [Cacna1c mice; referred to herein as α1[C.sup.+/-] mice]) and mice in which this gene was loxP targeted to achieve graded heart-specific gene deletion (termed herein α1C-loxP mice). Adult cardiomyocytes from the hearts of α1[C.sup.-/+] mice at 10 weeks of age showed a decrease in LTCC current and a modest decrease in cardiac function, which we initially hypothesized would be cardioprotective. However, α1[C.sup.+/-] mice subjected to pressure overload stimulation, isoproterenol infusion, and swimming showed greater cardiac hypertrophy, greater reductions in ventricular performance, and greater ventricular dilation than α1[C.sup.+/-] controls. The same detrimental effects were observed in α1C-loxP animals with a cardiomyocytespecific deletion of one allele. More severe reductions in α1C protein levels with combinatorial deleted alleles produced spontaneous cardiac hypertrophy before 3 months of age, with early adulthood lethality. Mechanisti-cally, our data suggest that a reduction in LTCC current leads to neuroendocrine stress, with sensitized and leaky sarcoplasmic reticulum [Ca.sup.2+] release as a compensatory mechanism to preserve contractility. This state results in calcineurin/nuclear factor of activated T cells signaling that promotes hypertrophy and disease., Introduction Voltage-gated L-type [Ca.sup.2+] channels (LTCCs) are the primary source of [Ca.sup.2+] influx to initiate cardiac excitation-contraction coupling (ECC) (1, 2). The molecular composition of the LTCC in cardiomyocytes includes [...]

Published
2012
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9. Facilitation of murine cardiac L-type [Ca.sub.v]1.2 channel is modulated by Calmodulin kinase II-dependent phosphorylation of S1512 and S1570

Author

Blaich, Anne, Welling, Andrea, Fischer, Stefanie, Wegener, Jorg Werner, Kostner, Katharina, Hofmann, Franz, and Moosmang, Sven

Subjects
Calmodulin -- Research, Calmodulin -- Physiological aspects, Calmodulin -- Genetic aspects, Calcium channels -- Research, Calcium channels -- Physiological aspects, Calcium channels -- Genetic aspects, Phosphorylation -- Physiological aspects, Phosphorylation -- Genetic aspects, Phosphorylation -- Research, Science and technology
Abstract

Activity-dependent means of altering calcium ([Ca.sup.2+]) influx are assumed to be of great physiological consequence, although definitive tests of this assumption have only begun to emerge. Facilitation and inactivation offer two opposing, activity-dependent means of altering [Ca.sup.2+] influx via cardiac [Ca.sub.v]1.2 calcium channels. Voltage- and frequency-dependent facilitation of [Ca.sub.v]1.2 has been reported to depend on Calmodulin (CAM) and/or the activity of Calmodulin kinase II (CaMKII). Several sites within the cardiac L-type calcium channel complex have been proposed as the targets of CaMKII. Here, we generated mice with knockin mutations of [[alpha].sub.1]1.2 S1512 and S1570 phosphorylation sites [sine facilitation (SF) mice]. Homocygote SF mice were viable and reproduced in a Mendelian ratio. Voltage-dependent facilitation in ventricular cardiomyocytes carrying the SF mutation was decreased from 1.58- to 1.18-fold. The CaMKII inhibitor KN-93 reduced facilitation to 1.28 in control cardiomyocytes. SF mutation negatively shifted the voltage-dependent inactivation and slowed recovery from inactivation, thereby making fewer channels available for activation. Telemetric ECG recordings at different heart rates showed that QT time decreased significantly more in SF than in control mice at higher rates. Our results strongly support the notion that CaMKII-dependent phosphorylation of [Ca.sub.v]1.2 at S1512 and S1570 mediates [Ca.sup.2+] current facilitation in the murine heart. calcium channels | facilitation | heart | voltage-dependent ion channels doi/ 10.1073/pnas.0914287107

Published
2010

13. Gastroenterologie

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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15. Schmerztherapie

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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16. Hämatologie

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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17. Ophthalmologie

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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18. Transplantationsmedizin

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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19. Dermatologie

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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20. Pneumologie

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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21. Infektiologie

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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22. Neurologie

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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27. Kardiologie, Angiologie

Author

Hofmann, Franz B., primary, Kleppisch, Thomas, additional, Moosmang, Sven, additional, and Wegener, Jörg W., additional

Published
2009
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32. Contributors

Author

ACKERMAN, MICHAEL J., primary, AGUEL, FELIPE, additional, ALBERTE-LISTA, CESAR, additional, ANTZ, MATTHIAS, additional, ANTZELEVITCH, CHARLES, additional, ANUMONWO, JUSTUS M.B., additional, ARORA, RISHI, additional, BACKX, PETER H., additional, BALSER, JEFFREY R., additional, BECKMAN, KAREN, additional, BENDITT, DAVID G., additional, BERBARI, EDWARD J., additional, BERENFELD, OMER, additional, BERS, DONALD M., additional, BEYER, ERIC C., additional, BIEL, MARTIN, additional, BOWLES, NEIL E., additional, BOYETT, MARK R., additional, BRUGADA, JOSEP, additional, BRUGADA, PEDRO, additional, BRUGADA, RAMON, additional, BURSAC, NENAD, additional, BUXTON, ALFRED E., additional, CAIN, MICHAEL E., additional, CALKINS, HUGH, additional, CALLANS, DAVID J., additional, CAPPATO, RICCARDO, additional, CARROLL, SHEILA J., additional, CASTELLANOS, AGUSTIN, additional, CHEN, LAN S., additional, CHEN, PENG-SHENG, additional, CHEN, SHIN-ANN, additional, CHEN, XIONGWEN, additional, CLAPHAM, DAVID E., additional, CLÉMENTY, JACQUES, additional, CRIJNS, HARRY J., additional, DAOUD, EMILE G., additional, DAS, MITHILESH K., additional, DELMAR, MARIO, additional, DIFRANCESCO, DARIO, additional, DIMARCO, JOHN P., additional, DOBRZYNSKI, HALINA, additional, DUFFY, HEATHER S., additional, EFIMOV, IGOR R., additional, EHRLICH, JOACHIM R., additional, EL-SHERIF, NABIL, additional, ELLENBOGEN, KENNETH A., additional, EPSTEIN, ANDREW E., additional, ERMIS, CENGIZ, additional, ERNST, SABINE, additional, ESTES, N. A. MARK, additional, FAST, VLADIMIR G., additional, FEDOROV, VADIM V., additional, FONTAINE, GUY, additional, FORESTI, SARA, additional, FORNES, PAUL, additional, FRANK, ROBERT, additional, FRANZ, MICHAEL R., additional, GALVIN, JOSEPH M., additional, GARFINKEL, ALAN, additional, GILLIS, ANNE M., additional, GOLD, MICHAEL R., additional, GOLDBERGER, JEFFREY, additional, GRAY, RICHARD A., additional, GRIMM, WOLFRAM, additional, GROH, WILLIAM J., additional, HAINES, DAVID E., additional, HAÏSSAGUERRE, MICHEL, additional, HARO, CARLOS, additional, HAYES, DAVID L., additional, HAYRAPETYAN, VOLODYA, additional, HEBERT, JEAN-LOUIS, additional, HENRIQUEZ, CRAIG S., additional, HERRMANN, STEFAN, additional, HINDRICKS, GERHARD, additional, HOCINI, MÉLÈZE, additional, HOFMANN, FRANZ, additional, HOHNLOSER, STEFAN H., additional, HONJO, HARUO, additional, HOUSER, STEVEN R., additional, HRYSHKO, LARRY V., additional, HSU, EDWARD W., additional, HUANG, JIAN, additional, HULOT, JEAN-SÉBASTIEN, additional, HUTCHINS, GARY D., additional, IDEKER, RAYMOND E., additional, INTERIAN, ALBERTO, additional, IWAI, SEI, additional, JACKMAN, WARREN M., additional, JAÏS, PIERRE, additional, JALIFE, JOSÉ, additional, JANUARY, CRAIG T., additional, JOHNSON, CHRISTOPHER R., additional, JOSEPHSON, MARK E., additional, JOUVEN, XAVIER, additional, KADISH, ALAN H., additional, KALMAN, JONATHAN M., additional, KAMP, TIMOTHY J., additional, KASS, ROBERT S., additional, KENNEDY, HAROLD L., additional, KERBER, RICHARD E., additional, KHOSITSETH, ANANT, additional, KILBORN, MICHAEL J., additional, KLÉBER, ANDRÉ G., additional, KLEIN, GEORGE J., additional, KNIGHT, BRADLEY P., additional, KODAMA, ITSUO, additional, KOTTKAMP, HANS, additional, KRAHN, ANDREW D., additional, KUCERA, JAN P., additional, KUCK, KARL-HEINZ, additional, KUGLER, JOHN D., additional, KUO, CHI TAI, additional, KUROKAWA, JUNKO, additional, LAB, MAX J., additional, LAI, WEN TER, additional, LARSON, CLAIRE, additional, LAURITA, KENNETH R., additional, LAZZARA, RALPH, additional, LERMAN, BRUCE B., additional, LERNER, DEBORAH L., additional, LÉVY, SAMUEL, additional, LI, RONALD A., additional, LIN, DAVID, additional, LOCKWOOD, DEBORAH, additional, LONDON, BARRY, additional, LÜ, FEI, additional, LUDWIG, ANDREAS, additional, MAKIELSKI, JONATHAN C., additional, MALIK, MAREK, additional, MARBÁN, EDUARDO, additional, MARCHLINSKI, FRANCIS E., additional, MARKIDES, VIAS, additional, MARKOWITZ, STEVEN M., additional, MARON, BARRY J., additional, MARTÍNEZ, AGUSTÍN D., additional, MCGUIRE, MARK A., additional, MEISSNER, GERHARD, additional, MILES, WILLIAM M., additional, MILLER, JOHN M., additional, MILLER, MICHAEL A., additional, MITTAL, SUNEET, additional, MOLEIRO, FEDERICO, additional, MOOSMANG, SVEN, additional, MORADY, FRED, additional, MORENO, ALONSO P., additional, MOSS, ARTHUR J., additional, MYERBURG, ROBERT J., additional, NAKAGAWA, HIROSHI, additional, NAPOLITANO, CARLO, additional, NATTEL, STANLEY, additional, NERBONNE, JEANNE M., additional, NIKOLSKI, VLADIMIR P., additional, OLGIN, JEFFREY E., additional, ORAL, HAKAN, additional, OTOMO, KENICHIRO, additional, OUDIT, GAVIN Y., additional, OUYANG, FEIFAN, additional, PAGÉ, PIERRE L., additional, PAPPONE, CARLO, additional, PATTERSON, EUGENE, additional, PERTSOV, ARKADY M., additional, PETERS, NICHOLAS S., additional, PETERS, ROBERT W., additional, PRIORI, SILVIA G., additional, PROST-SQUARCIONI, CATHERINE, additional, PRYSTOWSKI, ERIC N., additional, PUNSKE, BONNIE B., additional, QU, ZHILIN, additional, RAMIREZ, RAFAEL J., additional, RIVOLTA, ILARIA, additional, ROBINSON, RICHARD B., additional, RODEN, DAN M., additional, ROHR, STEPHAN, additional, ROSANIO, SALVATORE, additional, ROSEN, MICHAEL R., additional, ROSENBAUM, DAVID S., additional, ROSENSHTRAUKH, LEONID V., additional, ROTH, BRADLEY J., additional, RUDY, YORAM, additional, RUSKIN, JEREMY N., additional, SACHS, FREDERICK, additional, SAFFITZ, JEFFREY E., additional, SANDERS, PRASHANTHAN, additional, SANGUINETTI, MICHAEL C., additional, SAOUDI, NADIR, additional, SCHERLAG, BENJAMIN J., additional, SCHWARTZ, PETER J., additional, SCHWARTZMAN, DAVID, additional, SEGAL, OLIVER R., additional, SHAH, DIPEN C., additional, SHARIFOV, OLEG F., additional, SHIVKUMAR, KALYANAM, additional, SIMMONS, JEFFREY, additional, SINGH, BRAMAH N., additional, SKANES, ALLAN C., additional, SMITH, TIMOTHY W., additional, SOEJIMA, KYOKO, additional, SORGEN, PAUL L., additional, SPRAY, DAVID C., additional, SRINIVAS, MIDUTURU, additional, STEIN, KENNETH M., additional, STEINBERG, SUSAN F., additional, STEVENSON, WILLIAM G., additional, STIEBER, JULIANE, additional, STRAMBA-BADIALE, MARCO, additional, STRICKBERGER, S. ADAM, additional, SUNG, RUEY J., additional, SWEENEY, MICHAEL O., additional, SWERDLOW, CHARLES D., additional, TACCARDI, BRUNO, additional, TAFFET, STEVEN M., additional, TAI, CHING-TAI, additional, THOMAS, DANIEL, additional, TOMASELLI, GORDON F., additional, TONDATO, FERNANDO, additional, TOWBIN, JEFFREY A., additional, TRANQUILLO, JOSEPH V., additional, TRAYANOVA, NATALIA A., additional, TRIEDMAN, JOHN K., additional, TRISTANI-FIROUZI, MARTIN, additional, TSAI, CHIN-FENG, additional, TUNG, LESLIE, additional, TURITTO, GIOIA, additional, VAN HARE, GEORGE F., additional, VAN WAGONER, DAVID R., additional, VOS, MARC A., additional, WALCOTT, GREGORY P., additional, WALDO, ALBERT L., additional, WANG, ZULU, additional, WEINBERG, KENNETH M., additional, WEINSTEIN, DAVID, additional, WELLNER, MARCEL, additional, WILKOFF, BRUCE L., additional, WOOD, MARK A., additional, WU, JIANYI, additional, WU, JIASHIN, additional, WYSE, D. GEORGE, additional, YAMADA, KATHRYN A., additional, YE, BIN, additional, YEE, RAYMOND, additional, ZAITSEV, ALEXEY V., additional, ZAREBA, WOJCIECH, additional, ZHONG, GUOQIANG, additional, and ZIPES, DOUGLAS P., additional

Published
2004
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43. Remote and reversible inhibition of neurons and circuits by small molecule induced potassium channel stabilization

Author

Auffenberg, Eva, primary, Jurik, Angela, additional, Mattusch, Corinna, additional, Stoffel, Rainer, additional, Genewsky, Andreas, additional, Namendorf, Christian, additional, Schmid, Roland M., additional, Rammes, Gerhard, additional, Biel, Martin, additional, Uhr, Manfred, additional, Moosmang, Sven, additional, Michalakis, Stylianos, additional, Wotjak, Carsten T., additional, and Thoeringer, Christoph K., additional

Published
2016
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44. Tissue expression and cellular localization of pacemaker channels

Author

Moosmang, Sven, Hofmann, Franz (Prof. Dr.), Ruth, Peter Friedrich (Prof. Dr.), and Neumann, Franz-Josef Maria (Prof. Dr.)

Subjects
Medizin, ddc:610, Ionenkanal, Schrittmacherkanal, HCN, Kanal, Sinusknoten, Elektrophysiologie, Molekularbiologie, In-situ-Hybridisierung, ionic channel, pacemaker channel, channel, sinus node, electrophysiology, molecular biology, in situ hybridization
Abstract

Die rhythmische Aktivität von Schrittmacherzellen in Herz und Gehirn wird durch den Ih Strom gesteuert. Die molekulare Grundlage von Ih bilden die vier Mitglieder der HCN-Kanalfamilie. In dieser Arbeit wurde mit molekularbiologischen, biochemischen und histologischen Methoden die Expression von HCN1-4 im Herz, ZNS und dem peripheren Nervensystem untersucht. Im Sinusknoten wird besonders HCN4 exprimiert. Im Gehirn besitzt jeder der vier HCN-Kanalgene ein charakteristisches Verteilungsmuster. Die Heterogenität von nativem Ih kann somit mindestens teilweise durch die differentielle Expression der HCN-Kanäle erklärt werden. The rhythmic activity of pacemaker cells in heart and brain is controlled by the Ih current. The four members of the HCN channel family form the molecular basis of Ih. In this thesis, the expression of HCN1-4 in heart, ZNS and the peripheral nervous system was examined with molecular-biological, biochemical and histological methods. In the sino-atrial node, HCN4 is expressed particularly strong. In the brain each of the four HCN channel genes shows a characteristic distribution pattern. The heterogeneity of native Ih can thus be explained at least in part by the differential Expression of the HCN channels.

Published
2007

45. A Specific Role for the REV-ERBα–Controlled L-Type Voltage-Gated Calcium Channel CaV1.2 in Resetting the Circadian Clock in the Late Night

Author

Schmutz, Isabelle, primary, Chavan, Rohit, additional, Ripperger, Jürgen A., additional, Maywood, Elizabeth S., additional, Langwieser, Nicole, additional, Jurik, Angela, additional, Stauffer, Anja, additional, Delorme, James E., additional, Moosmang, Sven, additional, Hastings, Michael H., additional, Hofmann, Franz, additional, and Albrecht, Urs, additional

Published
2014
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46. Genetische Charakterisierung der Rolle von Calciumkanälen für die neuronale Entwicklung und Funktion

Author

Luksch, Harald (Prof. Dr.), Hofmann, Franz B. (Prof. Dr.), Frischmann, Dimitri (Prof. Dr.), Moosmang, Sven (Prof. Dr.), Jurik, Angela Maria, Luksch, Harald (Prof. Dr.), Hofmann, Franz B. (Prof. Dr.), Frischmann, Dimitri (Prof. Dr.), Moosmang, Sven (Prof. Dr.), and Jurik, Angela Maria

Abstract

Im Rahmen dieser Arbeit sollte die Wichtigkeit des IQ-Motivs des Cav1.2 Calciumkanals im Gehirn geklärt werden. Durch Generierung einer konditionalen, gehirnspezifischen Maus, die eine Mutation von Isoleucin zu Glutaminsäure im IQ-Motiv trägt, wurde gezeigt, dass durch diese Mutation die Proteinkonzentration des Cav1.2 Proteins stark reduziert wurde. Mäuse mit dieser Mutation zeigten eine erhöhte Angst vor neuen Umgebungen, anti-depressiv-ähnliches Verhalten und eine veränderte Angstadaption., The present work explored the importance of the IQ motif of the Cav1.2 calcium channel in brain. Therefore, a conditional brain specific mouse model was created, which carries a mutation from isoleucine to glutamate in the IQ motif. Here it has been shown, that this mutation reduced protein concentration of the Cav1.2 channel in a strong manner. Mice with this mutation showed enhanced anxiety in new environment, anti-depressive like behavior and modified anxiety adaptation.

Published
2013

47. Genetische Charakterisierung der Rolle von Calciumkanälen für die neuronale Entwicklung und Funktion

Author

Moosmang, Sven (Prof. Dr.);Hofmann, Franz B. (Prof. Dr.);Luksch, Harald (Prof. Dr.), Luksch, Harald (Prof. Dr.);Frischmann, Dimitri (Prof. Dr.);Hofmann, Franz B. (Prof. Dr.), Jurik, Angela Maria, Moosmang, Sven (Prof. Dr.);Hofmann, Franz B. (Prof. Dr.);Luksch, Harald (Prof. Dr.), Luksch, Harald (Prof. Dr.);Frischmann, Dimitri (Prof. Dr.);Hofmann, Franz B. (Prof. Dr.), and Jurik, Angela Maria

Abstract

Im Rahmen dieser Arbeit sollte die Wichtigkeit des IQ-Motivs des Cav1.2 Calciumkanals im Gehirn geklärt werden. Durch Generierung einer konditionalen, gehirnspezifischen Maus, die eine Mutation von Isoleucin zu Glutaminsäure im IQ-Motiv trägt, wurde gezeigt, dass durch diese Mutation die Proteinkonzentration des Cav1.2 Proteins stark reduziert wurde. Mäuse mit dieser Mutation zeigten eine erhöhte Angst vor neuen Umgebungen, anti-depressiv-ähnliches Verhalten und eine veränderte Angstadaption., The present work explored the importance of the IQ motif of the Cav1.2 calcium channel in brain. Therefore, a conditional brain specific mouse model was created, which carries a mutation from isoleucine to glutamate in the IQ motif. Here it has been shown, that this mutation reduced protein concentration of the Cav1.2 channel in a strong manner. Mice with this mutation showed enhanced anxiety in new environment, anti-depressive like behavior and modified anxiety adaptation.

Published
2013

48. Generierung und Analyse von Veränderungen im CACNB2 Gen

Author

Moosmang, Sven (Priv.-Doz. Dr.), Schemann, Michael (Prof. Dr.), Brandmayr, Julia, Moosmang, Sven (Priv.-Doz. Dr.), Schemann, Michael (Prof. Dr.), and Brandmayr, Julia

Abstract

Die Funktionen des CACNB2 Gens bei physiologischen und pathophysiologischen Prozessen im kardiovaskulären System sind bis dato ungeklärt, obwohl es viele Hinweise auf wichtige Aufgaben des Cavβ2-Proteins in vivo gibt. Im Rahmen der vorliegenden Arbeit sollen diese Aufgaben und Prozesse mit Hilfe von zwei neuartigen Mausmodellen beleuchtet werden. Das erste Modell, die Cavβ2STOP-Mauslinie, dient dazu, die Rolle der Cavβ2-Untereinheit bei Phosphorylierungskaskaden (PKA, CaMKII, Akt/PKB) zu analysieren. Erste biochemische und elektrophysiologische Experimente wurden durchgeführt, um die Relevanz der Phosphorylierungsstellen in vivo zu klären. Das zweite Modell, die Cavβ2STREP-Mauslinie, wurde generiert, um die Interaktionspartner und die damit verbundenen Signalwege der Cavβ2-Untereinheit systematisch, mit einem innovativen Kombinationssystem aus transgenen Technologien und einem neuartigen Affinitätsaufreinigungs-System, zu analysieren., The functions of the CACNB2 gene involved in physiological and pathophysiological processes in the cardiovascular system still remain unclear, although there is evidence that the Cavβ2 protein performs important tasks in vivo. The present work explores these processes and tasks by means of two novel knock-in mouse models. The first mouse model, the Cavβ2STOP-mouse, analyzes the role of the Cavβ2 subunit in phosphorylation cascades (PKA, CaMKII, Akt/PKB). Preliminary biochemical and electrophysiological experiments were initiated to resolve the relevance of these phosphorylation events in vivo. The second mouse model, the Cavβ2STREP mouse, was generated to systematically analyze the interaction partners and associated signaling pathways of the Cavβ2 subunit, by means of combining an innovative affinity purification system with transgenic in vivo technologies.

Published
2011

50. Analyse der Regulation von Kalziumkanälen über den Ca2+/CaM/CaMKII-Signalweg durch konditionale Mutagenese im Mausmodell

Author

Moosmang, Sven (Priv.-Doz. Dr.), Schemann, Michael (Prof. Dr.), Fischer, Stefanie, Moosmang, Sven (Priv.-Doz. Dr.), Schemann, Michael (Prof. Dr.), and Fischer, Stefanie

Abstract

Inaktivierung (CDI) und Fazilitierung (CDF) stellen die beiden Mechanismen der Autoregulation von Cav1.2-Kanälen dar. In vitro-Versuche deuten auf eine essentielle Bedeutung des I1624 für die Calmodulinbindung an den Kanal und somit für die Inaktivierung hin. Andere Mutationsstudien haben gezeigt, dass S1512 und S1570 für die über CaMKII-Aktivierung gesteuerte Fazilitierung entscheidend sind. Im Rahmen dieser Arbeit wurden zwei knock-in-Mauslinien generiert (Cav1.2_EQ und Cav1.2_SF) und somit die Grundlage geschaffen, erstmals CDI und CDF in vivo zu analysieren und ihre Bedeutung in einen physiologischen Gesamtzusammenhang zu bringen, um möglicherweise neue pharmakologische Behandlungsansätze für kardiale Erkrankungen, wie Herzinsuffizienz und Arrhythmien zu entdecken., Inactivation (CDI) and facilitation (CDF) are known mechanisms of autoregulation of Cav1.2 calcium channels. In vitro studies indicate an essential role of I1624 in binding of calmodulin to the channel causing its inactivation. Other mutagenesis studies show that S1512 and S1570 are the critical amino acids for CaMKII-mediated facilitation events. The aim of the present thesis was to generate two knock-in mouse lines (Cav1.2_EQ and Cav1.2_SF) to create a basis for in vivo studies concerning CDI and CDF of Cav1.2 calcium channels in a physiological setting. These models might help to elucidate new pharmacological treatment options for cardiac diseases, e.g. heart failure or arrhythmia.

Published
2009

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