Дисертації з теми "Kv3.3"
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Kemp, Laurens [Verfasser], Tobias [Akademischer Betreuer] Huth та Tobias [Gutachter] Huth. "Elektrophysiologische Untersuchung von Kv3.3/Kv3.4 Kanalkomplexen und deren Interaktion mit der β-Sekretase BACE1 / Laurens Kemp ; Gutachter: Tobias Huth ; Betreuer: Tobias Huth". Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2021. http://d-nb.info/1228627606/34.
Повний текст джерелаVallejo, Gracia Albert. "Kv1.3 and Kv1.5 channels in leukocytes." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/397797.
Повний текст джерелаRoig, Merino Sara Raquel. "Heteroligomeric interactions of the Kv1.3 channelosome." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/404756.
Повний текст джерелаSolé, i. Codina Laura. "Role of KCN E4 on the voltage gated potassium channel Kv1.3 = Paper de KCNE4 en el canal de potassi dependent de voltage Kv1.3." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/129685.
Повний текст джерелаEls canals de potassi dependents de voltatge (Kv) juguen un paper molt important tant en cèl•lules excitables com no excitables. La possibilitat de formar hetero-oligomers i la d’associació amb subunitats reguladores són uns dels mecanismes que existeixen per tal de proveir de diferents mecanismes per a respondre de manera diferent enfront a canvis en el potencial de membrana. La composició del canalosoma modula tant la seva expressió a superfície com l’activitat d’aquests. Aquesta tesi es centra en l’estudi de l’efecte del la família de les subunitats reguladores KCNE sobre diferents Kv. Primerament s’estudià l’efecte que causaven en el tràfic del canal Kv7.1 (canal model per a l’estudi dels KCNEs) i posteriorment s’amplià l’estudi a un altre membre de la mateixa família, Kv7.5. A continuació s’estudià un canal d’elevada importància per a l’activació i proliferació leucocitària: Kv1.3, centrant-nos sobretot en l’efecte causat per un dels KCNEs: KCNE4. Aquesta subunitat no només inhibeix dràsticament el corrent del canal Kv1.3, sinó que a més a més, modifica el seu tràfic i localització. Aquests canvis són deguts a una interacció directa entre ambdues proteïnes. A continuació s’estudià en detall el complex Kv1.3-KCNE4. Mitjançant la combinació d’experiments d’electrofisiologia i monitorització de fluorescència de molècules individuals en la membrana, es va poder establir l’estequiometria d’aquest complex. Posteriorment, mitjançant l’anàlisi de diverses proteïnes quimèriques i mutants, tant del canal com de la subunitat reguladora, es van cercar els determinants moleculars implicats en l’associació entre ambdues proteïnes. S’han pogut determinar els motius claus en KCNE4 i Kv1.3 implicats en la formació del complex, però no en la modulació del canal. Finalment, degut a la importància de Kv1.3 en el sistema immunitari, s’han analitzat els nivells d’expressió dels KCNEs en diferents línies leucocitàries. S’ha observat que aquestes subunitats pateixen una regulació diferencial en funció de la manera d’activació i al llarg de la proliferació del leucòcits, suggerint un possible paper en la regulació precisa de la resposta immunològica.
Schilling, Tom. "Morphologische, immunphänotypische und elektrophysiologische Eigenschaften deaktivierter muriner Mikroglia in vitro." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2001. http://dx.doi.org/10.18452/14649.
Повний текст джерелаMurine microglial cultures were deactivated with astrocyte-conditioned medium (ACM). The deactivation process was verified measuring morphological (ramification index) and immunological (expression level of adhesion molecules) parameters. By using macrophage-colony stimulating factor (M-CSF), granulocyte/macrophage-colony stimulating factor (GM-CSF), transforming growth factor beta (TGF-beta) and their corresponding antibodies it was shown, that to a different extent all of these cytokines influence the deactivation process of microglial cells by ACM. ACM treatment of microglial cultures also lead to a transient upregulation of a delayed potassium outward current. This upregulation was due to the impact of TGF-beta contained in ACM. The ACM induced potassium channel resembled in its kinetic and pharmacological properties the cloned Kv1.3 channel. Expression of Kv1.3 in microglial cells by TGF-beta or ACM was inhibited by the unspecific protein kinase inhibitor H7. These results show, that expression of Kv1.3 channels is not a special feature of activated microglia, which has been proposed in recent publications.
Arnoux, Isabelle. "Rôles et caractérisation de la microglie dans le développement du néocortex somatosensoriel de la souris." Phd thesis, Université René Descartes - Paris V, 2014. http://tel.archives-ouvertes.fr/tel-01070271.
Повний текст джерелаSerrano, Albarrás Antonio. "Heteromeric composition of the Kv 1.3 channelosome = Composició heteromèrica del canalosoma Kv1.3." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/665245.
Повний текст джерелаLos canales iónicos son proteínas transmembrana que contienen poros acuosos que permiten el paso de iones a través de la membrana plasmática a favor de gradiente electroquímico. Kv1.3 es un canal de potasio dependiente de voltaje de la superfamilia Shaker. La estructura básica consiste en una proteína con seis dominios transmembrana y el canal funcional está formado por cuatro copias de esta proteína. Kv1.3 participa en multitud de funciones del organismo: sistema nervioso, sistema inmunitario, señalización de la insulina o proliferación celular. En el sistema inmunitario está altamente expresado tanto en linfocitos como en fagocitos mononucleares. En ambos tipos celulares regula la activación inmunitaria y la proliferación celular. Además, se ve coexpresado con otras proteínas de relevancia como Kv1.5 o KCNE4. Kv1.5 puede heteromerizar con Kv1.3, dando lugar a heterotrámeros de estequiometrias variables. Por otro lado, KCNE4 puede interaccionar con Kv1.3, pero no con Kv1.5. Kv1.3 se ve potentemente inhibido por ambas asociaciones. En la presente tesis nos centramos en caracterizar estas interacciones y el peso de la estequiometría en sus efectos. Demostramos que ambas asociaciones tienen lugar en células del sistema inmunitario. Además, mediante una proteína de fusión logramos fijar la estequiometría del complejo Kv1.3-Kv1-5 en 1:1. Así, Kv1.5 demuestra ejercer como dominante negativo respecto a Kv1.3 en el complejo. Estas interacciones intramoleculares son estudiadas mediante el uso de diversas proteínas quiméricas para dilucidar el peso de los extremos carboxiterminales en la formación del canal y su función. Por otro lado, demostramos que KCNE4 afecta el canal de estequiometría 1:1 aumentado su actividad, en lugar de reducirla. Este descubrimiento presenta un nuevo paradigma en que la asociación con varias proteínas reguladoras puede resultar en la modificación del efecto de cada una de ellas. KCNE1 es una proteína reguladora al igual que KCNE4, pero que interactúa con Kv1.5. En la presente tesis demostramos como KCNE1 no solo interacciona con Kv1.5, sino que aumenta en gran medida su actividad. Finalmente, también genotipamos estos genes en pacientes de una enfermedad autoinmune como es la esclerosis múltiple, llegando a localizar diversos polimorfismos de posible interés fisiopatológico.
Venturini, Elisa [Verfasser], and Erich [Akademischer Betreuer] Gulbins. "Kv1.3 inhibitors in the treatment of glioma and melanoma / Elisa Venturini. Betreuer: Erich Gulbins." Duisburg, 2015. http://d-nb.info/108047885X/34.
Повний текст джерелаMartel, Julie. "Expression et caractérisation du canal potassique voltage-dépendant lymphocytaire Kv1.3 chez les cellules HEK 293." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq26390.pdf.
Повний текст джерелаMartel, Julie. "Expression et caractérisation du canal potassique voltage-dépendant lymphocytaire Kv1.3 chez les cellules HEK 293." Sherbrooke : Université de Sherbrooke, 1997.
Знайти повний текст джерелаBodendiek, Silke [Verfasser]. "4-Phenoxybutoxy-substituierte, anellierte Heterozyklen : Synthese und elektrophysiologische Testung am lymphozytären Kaliumkanal Kv1.3 / Silke Bodendiek." Kiel : Universitätsbibliothek Kiel, 2008. http://d-nb.info/1019670282/34.
Повний текст джерелаBezine, Maryem. "Implication du canal potassium Kv3.1 dans la lipotoxicité du 7-cétocholestérol, 24S-hydroxycholestérol et de l’acide tétracosanoïque sur des cellules nerveuses 158N et BV-2 : Etude des relations entre Kv3.1, homéostasie potassique et métabolisme peroxysomal dans la maladie d’Alzheimer." Thesis, Bourgogne Franche-Comté, 2017. http://www.theses.fr/2017UBFCI010/document.
Повний текст джерелаPotassium (K+) is involved in the regulation of cellular excitability, cell cycle regulation, cell viability, neuroprotection and maintenance of microglial and oligodendrocytic functions. Potassium dysfunction, described in several neurodegenerative diseases such as Alzheimer's Disease (AD), multiple sclerosis (MS), Parkinson's disease and Huntington's disease, may be a potential therapeutic target. The underlying toxic mechanisms of these neurodegenerative pathologies involve oxysterols, which are oxidized cholesterol derivatives, and fatty acids including those associated with peroxisomal metabolism. 7-ketocholesterol (7KC), 24S-hydroxycholesterol (24S-OHC) and tetracosanoic acid (C24:0), often found at increased levels in the brain and plasma of patients with neurodegenerative diseases (Nieman-Pick disease, MS, Parkinson's disease, Huntington's disease and X-ALD) lead to a breakdown of the redox equilibrium leading to neurodegeneration. In this context, it is interesting to determine the possible connection between the lipid environment and potassium homeostasis The in vitro study was carried out on 158N murine oligodendrocytes and microglial BV-2 cells. We have shown that the lipotoxicity of 7KC, 24S-OHC and C24:0 implies retention of K+ involving the voltage dependent potassium channels (Kv). These results have shown that inhibition of Kv channels lead to an increase in [K +] i contributing to the cytotoxicity of 7KC, 24S-OHC and C24:0. The retention of K+ induced by oxysterols (7KC and 24S-OHC) would be under the control of Kv3.1b. A clinical study, on plasma of patients with Alzheimer’s disease, revealed a negative correlation between docosahexaenoic acid (DHA) and K+ concentration. In the J20 mice, a transgenic model of Alzheimer’s disease, the expression of Kv3.1b and Abcd3 was decreased in the hippocampus and cortex. Overall, the results obtained established relationships between lipotoxicity, peroxisomal metabolism and potassium homeostasis in neurodegeneration and suggest a possible modulation of the expression and activity of kv3.1b in the pathophysiology of neurodegenerative diseases. So, modulation of Kv3.1 could constitute a new therapeuthic approach against some neurodegenerative diseases
Bassetto, Júnior Carlos Alberto Zanutto. "Estudo da atividade bloqueadora de N-Alquilbenzenossulfonamidas em canais iônicos, com enfase em canais para potássio." Universidade Estadual Paulista (UNESP), 2016. http://hdl.handle.net/11449/140287.
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Esta tese teve como objetivo estudar as moléculas orgânicas (N-alquilbenzenossulfonamidas) como inibidoras de canais para potássio do tipo KV3.1, heterologamente expressos em células L-929. Com o presente estudo constatou-se que as moléculas, N-alquilbenzenossulfonamidas, produzem efeitos inibitórios sobre KV3.1. Através da técnica de whole cell patch clamp, observou-se que os valores de IC50 para as moléculas que bloquearam o canal foram 13,5 μM, 16,9 μM, 25,9 μM, 34,2 μM, 34,9 μM e 60 μM, respectivamente, para 4-cloro-3-nitro-N-butilbenzenossulfonamida (SMD2), 4-cloro-3-nitro-N-furfutilbenzenossulfonamida (SMD3), 4-[N-(3’aminopropil)-2-pirrolidona]-3-nitro-N-butilbenzenossulfonamida (SMD2_APP), 4-[N-(3’aminopropil)-2-pirrolidona]-3-nitro-N-furfurilbenzenossulfonamida (SMD3_APP), 4-cloro-N-butilbenzenossulfonamida (SMD2_SN) e 4-cloro-N-furfurilbenzenossulfonamida (SMD3_SN). O efeito de todas as moléculas mostrou-se reversível quanto à ligação com o canal e todas atuaram como bloqueadores de canal aberto. Em SMD2, molécula que mostrou o menor valor de IC50, observou-se um deslocamento de -8 mV em relação ao controle, nas curvas de condutância versus voltagem, nas cinéticas de ativação e na recuperação a partir da inativação em relação à voltagem. O SMD2 não alterou as constantes de tempo de desativação, embora tenha mudado as constantes de ativação e inativação, além de ter induzido o fenômeno de tail crossover. Observou-se que para potenciais mais despolarizados, ocorreu o alívio do bloqueio (Block Relief). Não foi observado o efeito da dependência do pH para o bloqueio e SMD2 não mudou a seletividade do canal. Constatou-se que pulsos despolarizantes de curta duração induzem efeitos menos intensos, ao passo que pulsos despolarizantes mais longos, produzem efeitos mais intensos de SMD2 sobre o canal. Além disso, foi observado que, quanto mais o canal é usado, ou seja, aberto, mais ele é bloqueado por SMD2. Todos esses dados sugerem que SMD2 não interage com o estado fechado e nem com o estado inativado do canal, mas sim com seu estado aberto, apresentando também um efeito dependente de uso. De um ponto de vista farmacológico, isso indica que SMD2 pode ser uma molécula importante na modulação da atividade dos canais KV3.1, presentes em células com altas frequências de disparos de potencial de ação, podendo constituir uma nova classe de moduladores farmacológicos desses canais.
This thesis had the aim of studying the organic molecules (N-alkylbenzenesulfonamides) that block KV3.1 potassium channel heterologously expressed in L-929 cells. It was found that N-alkylbenzenesulfonamides have restrained effects on KV3.1. Through the whole cell patch clamp technique, it was observed that the values of IC50, for molecules that block the channel, were 13,5 μM, 16,9 μM, 25,9 μM, 34,2 μM, 34,9 μM and 60 μM, respectively 4-Chloro-3-nitro-N-butylbenzenesulfonamide (SMD2), 4-Chloro-3-nitro-N-furfurylbenzene-sulfonamide (SMD3), 4-[N-(3′-Aminopropyl)-2-pyrrolidone]-3-nitro-N-butylbenzenesulfona-mide (SMD2_APP), 4-[N-(3′-Aminopropyl)-2-pyrrolidone]-3-nitro-N-furfurylbenzene-sulfonamide (SMD3_APP), 4-Chloro-N-butyllbenzenesulfonamide (SMD2_SN) e 4-Chloro-N-furfurylbenzenesulfonamide(SMD3_SN). The effect of all molecules was reversible regards to the linking with the channel and all act as open channel blocker. In SMD2, molecule which showed the smallest value of IC50, it was observed a displacement of -8 mV compared to control, for conductance curves versus voltage, for the kinetics of activation and for the recovery from inactivation in relation to voltage. SMD2 did not change the deactivation of time constants, although it changed the activation and inactivation constants, and more, SMD2 have induced tail crossover phenomenon. It was observed that, for more depolarized potentials, there was a block relief. It was not observed the effect of pH dependence for the block and SMD2 did not change the channel selectivity. It was observed that, short duration depolarizing pulses prompt less intense effects, whereas long duration depolarizing pulses prompt more intense effects of SMD2 on the channels. Furthermore, it was observed that the more the channel is used, in an open state, the more it is blocked by SMD2. All of these data suggest that SMD2 does not interact neither with the closed state nor the inactivated state of channel, but with its open state presenting an use-dependent manner, also showing a use-dependent effect. In a pharmacological point of view, this indicates that SMD2 may be an important molecule in the modulation of the activity in the KV3.1 channels, presents in cells with high frequency of firing of action potential and may constitute a new class of pharmacological modulators.
Beck, Sascha Daniel. "Modulation des epithelialen Natriumkanals (ENaC) und des Shaker-Kaliumkanals Kv1.3 durch die Aldosteron-induzierte Serin-Threonin-Kinase SGK." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=96907915X.
Повний текст джерелаGroen, Christiane [Verfasser], and Robert [Akademischer Betreuer] Bähring. "Modulation des humanen rekombinanten Ito-Kanals Kv4.3/KChIP2 durch die zytoplasmatische Ca2+-Konzentration / Christiane Groen ; Betreuer: Robert Bähring." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2017. http://d-nb.info/1141904969/34.
Повний текст джерелаHandschuh, Juliane [Verfasser]. "The interaction of Kv1.3 with Dlg-like MAGUKs and its impact on calcium signaling in activated T cells / Juliane Handschuh." Magdeburg : Universitätsbibliothek, 2017. http://d-nb.info/1128726475/34.
Повний текст джерелаGrabert, Jochen. "Regulation of interneuronal voltage-gated potassium channels Kv3.1b and Kv3.2 and the calcium-binding protein parvalbumin in the rat visual cortex." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975799088.
Повний текст джерелаAlbers, Florian. "Identifikation charakteristischer Bindungsstrukturen zwischen den T-lymphozytären Kaliumkanälen Kv1.1, Kv1.3 und SKCa2 und Kanalliganden anhand von Chimären des prokaryotischen Kaliumkanals KcsA." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=974849731.
Повний текст джерелаCaballero, Martínez Amelia [Verfasser], and Elisabeth [Akademischer Betreuer] Deindl. "The role of the potassium channels KV1.3 and KCa3.1 in arteriogenic smooth muscle cell proliferation / Amelia Caballero Martínez ; Betreuer: Elisabeth Deindl." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1201274508/34.
Повний текст джерелаHaddjeri, Alexis. "Robustesse du phénotype électrique des neurones dopaminergiques de la substance noire compacte à la délétion des canaux potassium Kv4.3 et SK3." Thesis, Aix-Marseille, 2019. http://theses.univ-amu.fr.lama.univ-amu.fr/191211_HADDJERI_482kf140lioz770fao837wbiyys_TH.pdf.
Повний текст джерелаDuring my PhD, I precisely characterized the variations in electrical phenotype of the SNc DA neurons in Kv4.3 and SK3 KO animals, in physiological and pathophysiological conditions. In a first study, I analyzed a large number of electrophysiological parameters in these animals Combined with acute pharmacological blockade of these ion channels, I showed that Kv4.3 chronic deletion leads to a phenotypic change similar to the one induced by acute blockade of the channel while SK3 deletion appears to be compensated by other ion channels (in particular SK2). Motor behavior testing of Kv4.3 and SK3 KO animals confirmed the robustness of SK3 animals and the absence of robustness of Kv4.3 animals. In a second preliminary study, we used a bilateral partial lesion model to assess the behavioral and electrophysiological consequences of SK3 deletion on Parkinson's disease development. Our results suggest that in "Parkinson's" conditions, the chronic deletion of SK3 channel is associated with a slight anti-anxiety effect, the suppression of dopaminergic agonist hypersensitivity but also with motor deficits. From an electrophysiological viewpoint, the SNc DA neurons display a pacemaking behavior similar to the untreated condition. These two studies suggest that SNc DA neuron activity displays a partial and variable robustness to potassium channel deletion (robust to SK3 deletion, sensitive to Kv4.3 deletion) that can be revealed in physiological and pathophysiological conditions. This work will help understanding how ion channel mutations may alter SNc DA neuron vulnerability in Parkinson's disease
Brevet, Marie. "Diminution de l'expression du canal potassique Kv 1. 3 dans les adénocarcinomes mammaires et pancréatiques : Implication de la méthylation du gène Kv1.3." Amiens, 2008. http://www.theses.fr/2008AMIED013.
Повний текст джерелаPotassium (K+) channels play a crucial role in cell proliferation and apoptosis and are implicated in carcinogenesis. G-Protein Inwardly Rectifying K+ Channel 1 (Kir3. 1 or GIRK1) and the voltage-activated KV1. 3 channels are considered in this study. Using immunohistochemistry on 33 cancer and 31 normal breast samples, we showed an increase of GIRK1 and a decrease of KV1. 3 expression in breast cancer. Because methylation could repress gene transcription thereby affecting the protein expression, we hypothesized that KV1. 3 gene promoter was methylated in breast cancers. Methyl-specific PCR was realized on 52 breast cancers. Methylation of KV1. 3 gene promoter was observed in 42. 3% of breast cancers. This methylation was associated with a poor differentiation of the tumor. Immunohistochemical results performed on the same samples confirmed these results with a decrease of KV1. 3 expression especially in grade III tumors. Similar techniques were applied to pancreatic adenocarcinomas. As for breast cancer, GIRK1 expression increased and KV1. 3 expression decreased in pancreatic cancer as compare to normal pancreatic tissue. KV1. 3 promoter methylation was observed in 66. 1% of pancreatic cancers and this methylation seemed to be correlated with metastatic tumors and worse survival for the patients. This work demonstrates an aberrant expression of GIRK1 K+ channel in cancers and suggested that this channel may be used as pharmaceutical target. Finally, implication of KV1. 3 promoter methylation in breast and pancreatic carcinogenesis could permit new pharmaceutical products challenges as DNA methyltransferases inhibitors
Lange, Wienke [Verfasser], and Thomas [Akademischer Betreuer] Friedrich. "Untersuchungen zu Struktur und Funktion des Spannungssensors und regulatorischer Domänen im Bereich des Carboxy-Terminus von Kv7.3- und Kv7.4-Kanälen / Wienke Lange. Betreuer: Thomas Friedrich." Berlin : Universitätsbibliothek der Technischen Universität Berlin, 2011. http://d-nb.info/1014946670/34.
Повний текст джерелаReneer, Mary Catherine. "SIGNALING MECHANISMS INVOLVED IN THE GENERATION OF HUMAN PERIPHERAL iTREGS." UKnowledge, 2012. http://uknowledge.uky.edu/microbio_etds/5.
Повний текст джерелаValdor, Markus Verfasser], Hermann [Akademischer Betreuer] [Wagner, and Jens [Akademischer Betreuer] Kurreck. "Functional characterization of the Kv7.2/Kv7.3 ion channel in rat dorsal root ganglion neurons following RNA interference-based knockdown by viral gene transfer / Markus Valdor ; Hermann Wagner, Jens Kurreck." Aachen : Universitätsbibliothek der RWTH Aachen, 2018. http://d-nb.info/1171818645/34.
Повний текст джерелаValdor, Markus [Verfasser], Hermann [Akademischer Betreuer] Wagner, and Jens [Akademischer Betreuer] Kurreck. "Functional characterization of the Kv7.2/Kv7.3 ion channel in rat dorsal root ganglion neurons following RNA interference-based knockdown by viral gene transfer / Markus Valdor ; Hermann Wagner, Jens Kurreck." Aachen : Universitätsbibliothek der RWTH Aachen, 2018. http://d-nb.info/1171818645/34.
Повний текст джерелаGonzalez, Walter G. "Protein-Ligand Interactions and Allosteric Regulation of Activity in DREAM Protein." FIU Digital Commons, 2016. http://digitalcommons.fiu.edu/etd/2503.
Повний текст джерелаLeijon, Sara. "Molecular characterization of cholinergic vestibular and olivocochlear efferent neurons in the rodent brainstem." Thesis, Linköping University, Department of Physics, Chemistry and Biology, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-56844.
Повний текст джерелаThe neural code from the inner ear to the brain is dynamically controlled by central nervous efferent feedback to the audio-vestibular epithelium. Although such efference provides the basis for a cognitive control of our hearing and balance, we know surprisingly little about this feedback system. This project has investigated the applicability of a transgenic mouse model, expressing a fluorescent protein under the choline-acetyltransferase (ChAT) promoter, for targeting the cholinergic audio-vestibular efferent neurons in the brainstem. It was found that the mouse model is useful for targeting the vestibular efferents, which are fluorescent, but not the auditory efferents, which are not highlighted. This model enables, for the first time, physiological studies of the vestibular efferent neurons and their synaptic inputs. We next assessed the expression of the potassium channel family Kv4, known to generate transient potassium currents upon depolarization. Such potassium currents are found in auditory efferent neurons, but it is not known whether Kv4 subunits are expressed in these neurons. Moreover, it is not known if Kv4 is present and has a function in the vestibular efferent neurons. Double labelling with anti-ChAT and anti-Kv4.2 or Kv4.3 demonstrates that the Kv4.3 subunits are abundantly expressed in audio-vestibular efferents, thus indicating that this subunit is a large contributor to the excitability and firing properties of the auditory efferent neurons, and most probably also for the vestibular efferent neurons. In addition, we also unexpectedly found a strong expression of Kv4.3 in principal cells of the superior olive, the neurons which are important for sound localization.
Moussaud, Simon. "Etude de l'implication des cellules microgliales et de l'α-synucleine dans la maladie neurodégénérative de Parkinson". Phd thesis, Université de Bourgogne, 2011. http://tel.archives-ouvertes.fr/tel-00668186.
Повний текст джерелаMarks, David Ronald. "Kv1.3 modulation by PSD-95 and insulin." 2008. http://etd.lib.fsu.edu/theses/available/etd-07032008-124412.
Повний текст джерелаAdvisor: Debra Ann Fadool, Florida State University, College of Arts and Sciences, Dept. of Biological Science. Title and description from dissertation home page (viewed Sept. 17, 2008). Document formatted into pages; contains xiv, 217 pages. Includes bibliographical references.
Schmitz, Alexander. "Phenoxyalkoxypsoralene : eine neue Klasse hochpotenter Blocker des lymphozytären Kaliumkanals Kv1.3 /." 2004. http://www.gbv.de/dms/bs/toc/479946159.pdf.
Повний текст джерелаSchmidt-Lassen, Kristina. "Nicht-peptidische Blocker des lymphozytären Kaliumkanals Kv1.3 : Untersuchungen zu Struktur-Wirkungsbeziehungen /." 2005. http://www.gbv.de/du/services/toc/bs/486995119.
Повний текст джерелаFarah, Amin [Verfasser]. "Expression von Kv1.3-Kaliumkanälen in retinalen Pigmentepithelzellen / vorgelegt von Amin Farah." 2008. http://d-nb.info/98940157X/34.
Повний текст джерелаFang, Kung-Ping, and 范光平. "A study of voltage-gated potassium channel Kv3.4 during oral carcinogenesis." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/85857594845842206754.
Повний текст джерела國立陽明大學
口腔生物研究所
89
Potassium channel have been reported to be involved in the proliferation of many types of cells, including tumor cell lines. Mitogenic stimulation increases the level of expression of potassium channel in T lymphocytes and epithelial cells. In addition, drugs that block potassium channels inhibit the proliferation of mitogen-stimulated normal human T lymphocytes, malignant rat lymphoma cells, human melanoma cells and human breast cancer cells. The over expression of potassium channel and related activity have been observed in neoplasms. Oral cancer is the fifth most common malignancy of the male population in Taiwan and more than 90 % of that are oral squamous cell carcinoma(OSCC) and the incidence and mortality of OSCC are increasing year by year. Our previous studies have shown that the abnormal expression of a voltage-gated potassium channel, Kv3.4 in an OSCC cell line by differential display. Preliminary studies also indicated the differential expression of Kv3.4 in normal appealing oral tissue and OSCC both in mRNA and protein level. We constructed the expression vector carring the Kv3.4 coding sequence, transfected into the OSCC cell line OEC-M1 and determined the high expression of Kv3.4 for subsequent carcinogenic studies. Our results suggest that the increasing expression of Kv3.4 may be beneficial for the cell growth without altering the cell cycle pattern of cancer cells. In addition, over expressing of Kv3.4 increased the chemoreistance of cancer cells. Although, Kv3.4 can not transform the 3T3 cells excluded the direct contribution of Kv3.4 in cell transformation, The potential role of Kv3.4 in carcinogenesis deserved further investigation.
Dreker, Tobias. "Untersuchung der Verapamil-Bindungsstelle des spannungsabhängigen Kaliumkanals Kv1.3 mit Hilfe von Phenylalkylaminsonden /." 2006. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=015032559&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
Повний текст джерелаHsu, Yi-Hua, and 許益華. "Expression of A-type K+ Channel Kv4.3 in Rat Cerebellum during Development." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/15443287374723611701.
Повний текст джерела國立陽明大學
神經科學研究所
90
Kv4.3, a voltage-gated potassium channel alpha subunit, can evoke A-current in Xenopus oocytes. Previous studies showed that Kv4.3 mRNA exhibited an anterior-posterior (A-P) compartmentalization in granular layer of rat cerebel- lum. Kv4.3 mRNA was highly expressed in the posterior lobules, but at low levels in the anterior lobules. Kv4.3 has been the only ion channel subunit exhibiting A-P compartmentalization in mammalian cerebellum known so far. However, details related to this A-P compartmentalization, as well as the spatial and temporal expression of Kv4.3 in the cerebellum, remained unclear. In this study, with immunohistochemistry and double immunofluorescent staining, we found that granule cell is the only cell type responsible for the A-P compartmen- talization. Kv4.3 was expressed in the somata of posterior granule cells soon after they migrated from the external germinal layer into the internal granular layer at early postnatal stage. Kv4.3 was concentrated on the dendrites after granule cell maturation. Kv4.3 was not expressed in the germinal trigone or the external germinal layer, where granule cell precursors are located. Interestingly, we found that Kv4.3 was transiently expressed in migrating Purkinje cells at em- bryonic stage, and the expression pattern was complementary to calbindin staining. In contrast, in the basket cells, stellate cells, Lugaro cells, a subpopu- lation of Golgi cells, and a subset of deep neurons, expression of Kv4.3 was started soon after they arrived at their final destinations and continued through- out adulthood. Kv4.3 was selectively expressed in posterior but not anterior granule cells, suggesting that anterior and posterior granule cells are derived from two different populations of precursors. Transient expression of Kv4.3 in migrating Purkinje cells suggests that Kv4.3 may be important for the migration of Purkinje cells. Expression of Kv4.3 in many types of cerebellar inter- neurons suggests that Kv4.3 could be crucial for modulating signals in the cerebellum.
Chang, Yu-Cheng, and 張宇晟. "Increased expression of Kv4.3 channel complex in nociceptors reduces peripheral neuropathic pain." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/80811175800238951774.
Повний текст джерела國立陽明大學
神經科學研究所
103
Kv4 channels, a subfamily of voltage-gated K+ (Kv) channels that evoke A-type potassium currents, play a crucial role in controlling neuronal excitability. Accumulative evidence suggest that native Kv4 channels function in ternary complex comprising Kv4 α-subunits and accessory β-subunits, including cytosolic Kv channel-interacting proteins (KChIPs) and transmembrane dipeptidyl peptidase-like proteins (DPPLs). Compared with Kv4 α-subunits alone, A-type potassium currents are robustly increased when they are coexpressed with β-subunits in heterologous systems. Neuropathic pain is often induced by peripheral nerve injury. Our previous studies have demonstrated that Kv4.3 is expressed in the somata of a subset of non-peptidergic nociceptors within the dorsal root ganglion (DRG), Kv4.3 protein level is greatly reduced after peripheral nerve injury, and knockdown of Kv4.3 expression in nociceptors can induce pain in naïve rats. Here, to investigate whether increasing Kv4.3 protein level can relieve neuropathic pain, we used unilateral L5/L6 spinal nerve ligation (SNL) in rats as an animal model. Kv4.3 cDNA was transfected into rat lumbar DRG neurons by a nonviural vector polyethylenimine (PEI) through intrathecal injection. Intrathecal injection of Kv4.3 cDNA slightly attenuated SNL-induced mechanical hypersensitivity (a major symptom of neuropathic pain) by increasing Kv4.3 protein expression in the ipsilateral L5/L6 DRGs. In addition, co-injection of Kv4.3 and its auxiliary subunit cDNAs greatly attenuated SNL-induced mechanical hypersensitivity. Furthermore, SNL-induced nociceptor activity is reduced more by Kv4.3/KChIP1/DPP10 cDNAs than by Kv4.3 cDNA alone. These data suggest that Kv4.3 and its auxiliary subunits KChIP1/DPP10 are potential targets for treating peripheral neuropathic pain.
Lin, Ming-Xin, and 林明勳. "Transient expression of Kv3.4 potassium channel in migrating hippocampal neurons during development." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/13585157340727202043.
Повний текст джерела國立陽明大學
神經科學研究所
95
Neuronal migration is essential for the establishment of normal brain organization during development. Hippocampus is the key brain region for learning and memory. Malformation of hippocampus will result in mental retardation and epilepsy in children. Kv3 channels, a group of voltage-gated K+ (Kv) channels, are required for repetitive firing at high frequency in mature neurons. Recent studies indicated that Kv3 channels were expressed in migrating neurons during chick hindbrain formation. To investigate the role of Kv3 channels in neuronal migration, a useful first step was to map their distributions in rat hippocampus at various developmental stages by immunohistochemistry. We found that Kv3.4 was expressed in new born neurons migrating radially from the ventricular zone to the primordial plexiform layer during the embryonic day E12.5~E15.5. In addition, Kv3.4 appeared in a stream of GABAergic interneurons, which originate from the striatum, migrate tangentially via cerebral cortex, and finally arrive at hippocampus during E15.5~E19.5. Interestingly, Kv3.4 disappeared from both radially and tangentially migrating neurons soon after they arrived at the destinations. In summary, Kv3.4 was transiently expressed in both the radially and tangentially migrating neurons during the development of hippocampus. Our data suggest that dysfunction of Kv3.4 may result in mental retardation and epilepsy in children, due to the malformation of hippocampus during pregnancy. In contrast, Kv3.3 was expressed in parvalbumin- and somatostatin-positive interneurons located in the pyramidal cell layer since the postnatal day 9. These Kv3.3(+) neurons also co-expressed Kv3.1b or Kv3.2. These results suggest that Kv3.3, as well as Kv3.1b and Kv3.2, may protect us from epilepsy resulted from neuronal over-excitation in the hippocampus since the early postnatal stage.
Ku, Wen-Xin, and 古文昕. "Pharmacophore- and structure-based virtual screening of potential Kv1.3 inhibitors with new scaffolds." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/mtn4zz.
Повний текст джерела國立臺北科技大學
生物科技研究所
99
In addition to KCa3.1, Kv1.3 has been regarded as a promising target for the selective inhibition of terminally differentiated effector memory T (TEM) cell in T cell-mediated autoimmune diseases, such as multiple sclerosis and type 1 diabetes. In this study, pharmacophore-based virtual screening was used to search for new lead compounds with new scaffolds that can serve as potential drugs without causing liver toxicity. A total of 106 Kv1.3 inhibitors, which were collected from published literatures, were used to build pharmacophore model. The best pharmacophore model (Hypo3-3), containing of two hydrogen bond acceptor, one hydrophobic, and one aromatic ring, has the highest R2 value (0.763) for the test set. The cross validation method with 95% confidence level was further used to validate Hypo3-3 and proved that this model was reliable in identifying structurally diverse compounds for Kv1.3 inhibition. This model was then employed as a filter to search for lead compounds with new scaffolds from the NCI chemical database. Top 10 hit compounds, selected based on their fit values, were found to share different conformations. On the other hand, the potent and selective Kv1.3 inhibitors can be retrieved by structure-based virtual screening. In the beginning, the Kv1.3 structure was build by homology modeling using the highest resolution structure of Kv1.2 as the template. Then, PAP-1, Psora-4 and 7-substituted khelliones inhibitors with selectivity for Kv1.3 were collected to construct a consensus scoring function with highly predicative ability by molecular docking. After docking ligand from commercially available database, this consensus scoring function was used to discover the novel selective Kv1.3 inhibitors. The resulting hit compounds from both ligand- and structure-based virtual screening can be applied in further in vitro biological evaluation and optimization.
Amadi, Chiemezie Chianotu. "Attenuation of extracellular potassium concentration effects on cardiac Kv4.3 gating, by conventional KChIP2 isoforms." 2005. http://proquest.umi.com/pqdweb?did=974428841&sid=22&Fmt=2&clientId=39334&RQT=309&VName=PQD.
Повний текст джерелаTitle from PDF title page (viewed on Mar. 21, 2006) Available through UMI ProQuest Digital Dissertations. Thesis adviser: Campbell, Donald L. Includes bibliographical references.
Ahmed, Ishtiaq. "Ensnaring the pancreatic alpha-cell, and, Syntaxin 1A modulation of the alpha-cell Kv4.3 channel." 2006. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=442243&T=F.
Повний текст джерелаSkrobek, Lennart [Verfasser]. "Biophysikalischer Einfluss von Kv6.1-, Kv6.3- und Kv6.4-Proteinen auf den spannungsabhängigen Kaliumkanal Kv2.1 / vorgelegt vonLennart Skrobek." 2008. http://d-nb.info/98994431X/34.
Повний текст джерелаHuang, Chia-Yi, and 黃嘉怡. "Transient expression of A-type K+ channel Kv3.4 in early axonal tracts of developing rat forebrain." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/22270560335509082181.
Повний текст джерела國立陽明大學
神經科學研究所
97
The formation of functional neuronal circuits depends on precise axon wiring during development. Appropriate wiring of forebrain circuits is necessary for intellectual, social and emotional dimensions of behavior. Previous studies have found that potassium channels are required for axon extension and guidance of Xenopus retinal ganglion cells in vitro. However, little is known about the spatiotemporal distribution of potassium channels in developing forebrain circuits. In this study, we focus on Kv3.4, an A-type potassium channel, which is important in controlling neuronal spike frequency. Kv3.4 appears more frequently in the axons and nerve terminals of adult brain neurons. To investigate whether Kv3.4 is expressed in growing axons in vivo, we have mapped Kv3.4 in embryonic rat forebrain by immunohistochemistry. Spatially, Kv3.4 is widely expressed in early axonal tracts, such as the lateral olfactory tract, optic nerves, corticofugal fibers, hippocamposeptal projection, and thalamocortical axons. Temporally, Kv3.4 appears in these axonal tracts only during embryonic day (E)14.5-E20.5, a time period coincides with early axon outgrowth. Furthermore, although these early axonal tracts remain visible around birth (E22 in rat), Kv3.4 has become undetectable from them, indicating that Kv3.4 disappears from axons before axons refine synaptic connections with their targets. DCC (deleted in colorectal cancer), a receptor for the axon guidance cue netrin-1, is largely confined to early axonal tracts and crucial for axon guidance. Ca2+ influx through L-type Ca2+ channel mediates axon outgrowth induced by netrin-1. Interestingly, Kv3.4 is co-localized with DCC and Cav1.2 in all early axonal tracts examined during E14.5-E20.5. Taken together, Kv3.4 is expressed in early axonal tracts widely during the phase of axon outgrowth/guidance, implicating that Kv3.4 may regulate axon outgrowth via controlling neuronal spike frequency.
Huang, Chia-Yi, and 黃嘉怡. "K+ channel Kv3.4 is essential for axon growth by limiting the influx of Ca2+ into growth cones." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/4mrg66.
Повний текст джерела國立陽明大學
神經科學研究所
105
Membrane excitability in the axonal growth cones of embryonic neurons influences axon growth. Voltage-gated K+ (Kv) channels are key factors in controlling membrane excitability, but whether they regulate axon growth remains unclear. Here, we report that Kv3.4 is expressed in the axonal growth cones of embryonic spinal commissural neurons, motoneurons, dorsal root ganglion neurons, retinal ganglion cells and callosal projection neurons during axon growth. Our in vitro (cultured dorsal spinal neurons of chick embryos) and in vivo (developing chick spinal commissural axons and rat callosal axons) findings demonstrate that knockdown of Kv3.4 by a specific shRNA impedes axon initiation, elongation, pathfinding, and fasciculation. In cultured dorsal spinal neurons, blockade of Kv3.4 by blood depressing substance II (BDSII) suppresses axon growth via an increase in the amplitude and frequency of Ca2+ influx through T-type and L-type Ca2+ channels. Electrophysiological results show that Kv3.4, the major Kv channel in the axonal growth cones of embryonic dorsal spinal neurons, is activated at more hyperpolarized potentials and inactivated more slowly than it is in postnatal and adult neurons. The opening of Kv3.4 channels effectively reduces growth cone membrane excitability, thereby limiting excessive Ca2+ influx at subthreshold potentials or during Ca2+-dependent action potentials. Furthermore, excessive Ca2+ influx induced by an optogenetic approach also inhibits axon growth. Interestingly, knockdown of Wnt3a reduces Kv3.4 expression in developing spinal commissural axons. Our findings suggest that Kv3.4 reduces growth cone membrane excitability and maintains [Ca2+]i at an optimal concentration for normal axon growth.
Vennekamp, Julia [Verfasser]. "Synthese und elektrophysiologische Testung hochwirksamer Psoralenderivate als nicht-peptidische Blocker des lymphozytären Kaliumkanals Kv1.3 / vorgelegt von Julia Vennekamp." 2002. http://d-nb.info/972280251/34.
Повний текст джерелаYang, Jung-Hui, and 楊榮慧. "Induction of Mechanical Pain by Interdependent Downregulation between K+ Channel Kv4.3 and Accessory KChIP1 in Pain-Sensing Neurons." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/90509963481417683197.
Повний текст джерела國立陽明大學
神經科學研究所
100
Kv4 channels evoke A-type K+ currents which play a critical role in regulating neuronal excitability. Native Kv4 channels function in complex comprising Kv4 α-subunits and accessory β-subunits, such as cytosolic K+ channel interacting proteins (KChIPs) and transmembrane dipeptidyl peptidase like proteins (DPPLs). Compared with Kv4 α-subunits alone, A-type K+ currents are robustly increased when they are co-expressed with accessory β-subunits in heterologous systems. The protein expression of Kv4 α- or β- subunits affect protein levels of the other. However, the related physiological significance has not been explored. Kv4.3, one of the Kv4 α-subunits, is expressed selectively in the cell bodies of a subset of pain-sensing neurons and its down-regulation induces mechanical pain. In this study, we found that KChIP1 and Kv4.3 were co-expressed in a subset of pain-sensing neurons. In a neuropathic pain model induced by lumbar spinal nerve ligation in the rat, the protein level of KChIP1 was reduced in pain-sensing neurons, same as that of Kv4.3. After knockdown either KChIP1 or Kv4.3 expression by intrathecal injection of gene-specific antisense oligonucleotide, KChIP1 and Kv4.3 protein levels were simultaneously decreased in pain-sensing neurons and mechanical hypersensitivity was induced. We also examined that knockdown effect of another Kv4 β-subunit DPP10, whose mRNA has been detected in the DRG. Our data showed that mechanical hypersensitivity was induced although Kv4.3 protein level was not affected. These data reveal that after decreasing either KChIP1 or DPP10 β-subunit in the DRG, mechanical pain develops. Kv4.3 and KChIP1 protein levels are co-dependent, whereas DPP10 and Kv4.3 protein levels are not.
Wernekenschnieder, Anja [Verfasser]. "Untersuchungen zu den inhibitorischen Wirkungen von Curcumin- und Psoralen-Derivaten auf den lymphozytären Kaliumkanal Kv1.3 / vorgelegt von Anja Wernekenschnieder." 2003. http://d-nb.info/972286160/34.
Повний текст джерелаBeck, Sascha Daniel [Verfasser]. "Modulation des epithelialen Natriumkanals (ENaC) und des Shaker-Kaliumkanals Kv1.3 durch die Aldosteron-induzierte Serin-Threonin-Kinase SGK / vorgelegt von Sascha Daniel Beck." 2003. http://d-nb.info/96907915X/34.
Повний текст джерелаHenne, Jutta. "Untersuchung zur Veränderung der Aktionspotentialmuster während der Reifung von Forellen Retina Ganglienzellen (Oncorhynchus mykiss) unter besonderer Berücksichtigung Kv3.1 und B k verwandter Kaliumkanäle." Doctoral thesis, 2005. https://repositorium.ub.uni-osnabrueck.de/handle/urn:nbn:de:gbv:700-2005051113.
Повний текст джерелаGrabert, Jochen [Verfasser]. "Regulation of interneuronal voltage-gated potassium channels Kv3.1b and Kv3.2 and the calcium-binding protein parvalbumin in the rat visual cortex / submitted by Jochen Grabert." 2005. http://d-nb.info/975799088/34.
Повний текст джерелаAlbers, Florian [Verfasser]. "Identifikation charakteristischer Bindungsstrukturen zwischen den T-lymphozytären Kaliumkanälen Kv1.1, Kv1.3 und SKCa2 und Kanalliganden anhand von Chimären des prokaryotischen Kaliumkanals KcsA / vorgelegt von Florian Albers." 2005. http://d-nb.info/974849731/34.
Повний текст джерела