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Thèses sur le sujet « GIRK channels »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 19 février 2022

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1

Nassirpour, Rounak. "Regulators of neuronal GIRK channels." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3307328.

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Thesis (Ph. D.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed July 11, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.

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2

ZHANG, Liyan. "Mechanosensitivity of GIRK Channels Depends on Channel-PIP_2 Interactions(RIEM Conference II, 2002)." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2805.

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3

Aryal, Prafulla. "Insights into mechanism of alcohol mediated modulation of GIRK channels." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p3390890.

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Thesis (Ph. D.)--University of California, San Diego, 2010.<br>Title from first page of PDF file (viewed Feb. 19, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.

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4

Jaén, Cristina. "Differential coupling of RGS3s and RGS4 to GPCR-GIRK channel signaling complexes." [Tampa, Fla] : University of South Florida, 2006. http://purl.fcla.edu/usf/dc/et/SFE0001533.

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5

ZHANG, Liyan, Jong-Kook LEE, and Itsuo KODAMA. "Molecular Mechanisms for Regulation of the G Protein-activated Inwardly Rectifying K^+ (GIRK) Channels by Protein Kinase C." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2791.

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6

Mahajan, Rahul. "Gβγ acts at an inter-subunit cleft to activate GIRK1 channels". VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/3307.

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Heterotrimeric guanine nucleotide-binding proteins (G-proteins) consist of an alpha subunit (Gα) and the dimeric beta-gamma subunit (Gβγ). The first example of direct cell signaling by Gβγ was the discovery of its role in activating G-protein regulated inwardly rectifying K+ (GIRK) channels which underlie the acetylcholine-induced K+ current responsible for vagal inhibition of heart rate. Published crystal structures have provided important insights into the structures of the G-protein subunits and GIRK channels separately, but co-crystals of the channel and Gβγ together remain elusive and no

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7

Ha, Junghoon. "Hydrogen Sulfide Regulation of Kir Channels." VCU Scholars Compass, 2017. https://scholarscompass.vcu.edu/etd/5204.

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Inwardly rectifying potassium (Kir) channels establish and regulate the resting membrane potential of excitable cells in the heart, brain and other peripheral tissues. Phosphatidylinositol- 4,5-bisphosphate (PIP2) is a key direct activator of ion channels, including Kir channels. Gasotransmitters, such as carbon monoxide (CO), have been reported to regulate the activity of Kir channels by altering channel-PIP2 interactions. We tested, in a model system, the effects and mechanism of action of another important gasotransmitter, hydrogen sulfide (H2S) thought to play a key role in cellular respon

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8

Irie, Tomohiko. "Activation of GIRK channels by muscarinic receptors and group 2 metabotropic glutamate receptors suppresses Golgi cell activity in the cochlear nucleus of mice." Kyoto University, 2008. http://hdl.handle.net/2433/135798.

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9

Yang, Chul Ho. "Paired Interactions between Kir channels and Tertiapin-Q." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3183.

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Kir channels serve diverse and important roles throughout the human body and malfunctions of these channels are implicated in various channelopathies. Specific inhibitors for different subtypes of Kir channels are not available. However, Tertiapin-Q (TPNQ), a polypeptide isolated from honey bee venom, differentially inhibits certain subtypes of Kir channels with nanomolar affinity: ROMK1 (Kir1.1) and GIRK1/GIRK4 (Kir3.1/Kir3.4). Modification of TPNQ to increase selectivity for target channels bears great therapeutic potential. The in silico studies based on TPNQ-docked channel models, ROMK1_IR

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10

Jaén, Cristina. "Differential coupling of RGS3s and RGS4 to GPCR-GIRK channel signaling complexes." Scholar Commons, 2006. http://scholarcommons.usf.edu/etd/2571.

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'Regulators of G protein signaling' (RGS proteins) modulate the G proteincycle by enhancing the GTPase activity of Ga subunits. These changesaccelerate the kinetics of ion channel modulation by Gai/o-coupled receptors(GPCRs) such as the G protein-gated inward rectifier K+ (GIRK/Kir3) channel. Myexperiments indicate that a single cerebellar granule (CG) neuron, a cell type thatendogenously expresses GIRK channels is able to express a wide variety ofRGS proteins. I selected two of them, which are widely expressed andtranscriptionally regulated during pathophysiologic conditions, to compare their

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11

Adney, Scott. "Protein Kinase C Dependent Inhibition of Kir3.2 (GIRK2) Channel Activity and Its Molecular Determinants." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3214.

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Inwardly rectifying potassium (Kir) channels are critically important for regulating resting membrane potential in excitable cells, a job underscored by the severe pathophysiology associated with channel dysfunction. While all Kir channels require the activating lipid PIP2, many of these channels have diverse modulatory factors that couple to PIP2-dependent gating. Channels in the Kir3 (GIRK) family, in particular, have several co-activating elements, including G-protein betagamma subunits, ethanol, and sodium. During stimulation of Gq-coupled receptors, downstream activation of Protein Kinase

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12

Mahajan, Rahul. "Gbetagamma acts at an inter-subunit cleft to activate GIRK1 channels." Thesis, Virginia Commonwealth University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3614785.

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<p> Heterotrimeric guanine nucleotide-binding proteins (G-proteins) consist of an alpha subunit (G&agr;) and the dimeric beta-gamma subunit (Gβγ). The first example of direct cell signaling by Gβγ was the discovery of its role in activating G-protein regulated inwardly rectifying K<sup> +</sup> (GIRK) channels which underlie the acetylcholine-induced K<sup> +</sup> current responsible for vagal inhibition of heart rate. Published crystal structures have provided important insights into the structures of the G-protein subunits and GIRK channels separately, but co-crystals

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13

Tomczyńska, Magdelena. "Biologie de l'endothélium vasculaire isolé de souris transgéniques YAC67 et YAC84- modèles murins du syndrome de Down." Thesis, Orléans, 2009. http://www.theses.fr/2009ORLE2067/document.

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GIRK2 est situé sur le chromosome 21, dont la trisomie cause le syndrome de Down (DS). Les proportionss des sous-populations de lymphocytes T sont altérées, le nombre de lymphocytes B circulants est diminué. Notre hypothèse est un défaut de contrôle de la domiciliation/recirculation des leucocytes par les cellules endothéliales (CE). Les CE formant la paroi des vaisseaux, assurent la néovascularisation, interagissent avec les cellules circulantes, initient l’adhésion donc, la réponse immune. Pour élucider l’influence de GIRK2 sur la fonction des CE, un modèle cellulaire in vitro a été mis au p

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14

Freitas, Josiane da Silva. "Estudo computacional de efeitos de alterações nas condutâncias de canais iônicos sobre a atividade elétrica de modelos morfologicamente realistas de células granulares do giro denteado do hipocampo de ratos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-01072016-141400/.

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A ocorrência de status epileticus (SE) desencadeia algumas alterações no sistema nervoso central. O giro denteado (GD) do hipocampo sofre com modificações na expressão gênica dos canais iônicos das células granulares (CGs) e essas células sofrem alterações morfológicas. Essas alterações se manifestam com o brotamento de fibras musgosas, redução no número de espinhas dendríticas, encurtamento e estreitamento da arborização dendrítica. As modificações na expressão gênica dos canais iônicos afetam suas densidades máximas de condutância. Este estudo utilizou 40 modelos computacionais realistas par

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15

Murphy, Joseph Francis. "Possible role of phosphorylation and cytoplasmic factors in the regulation of functionally expressed GIRK/CIR channels /." 1997. http://wwwlib.umi.com/dissertations/fullcit/3178380.

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16

Timpert, Mathias [Verfasser]. "A FRET-based approach for studying desensitization of G protein-activated K+(GIRK) channels / by Mathias Timpert." 2010. http://d-nb.info/1004293429/34.

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17

Hance, Michael W. "The Effects of 17- Beta Estradiol on G-Protein Inwardly Rectifying Potassium Channels (GIRKs) in Breast Cancer." 2009. http://trace.tennessee.edu/utk_graddiss/41.

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Breast cancer is a leading cause of cancer death and in 2009, the American Cancer Society estimates that over 192,000 new cases of breast cancer will be diagnosed, and over 40,000 women will die from breast cancer. Estrogen (E2) is required for normal female development and reproduction, but long-term exposure is carcinogenic and considered a risk factor for breast cancer. Membrane ion channels are essential for cell proliferation and are suggested to have a role in cancer, especially potassium channels. In the present study, we investigate the effects of estrogen and the estrogen antagonist I

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