Relevant bibliographies by topics / Kir3

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Kir3'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Kir3"

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Hibino, Hiroshi, Atsushi Inanobe, Kazuharu Furutani, Shingo Murakami, Ian Findlay, and Yoshihisa Kurachi. "Inwardly Rectifying Potassium Channels: Their Structure, Function, and Physiological Roles." Physiological Reviews 90, no. 1 (2010): 291–366. http://dx.doi.org/10.1152/physrev.00021.2009.

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Inwardly rectifying K+(Kir) channels allow K+to move more easily into rather than out of the cell. They have diverse physiological functions depending on their type and their location. There are seven Kir channel subfamilies that can be classified into four functional groups: classical Kir channels (Kir2.x) are constitutively active, G protein-gated Kir channels (Kir3.x) are regulated by G protein-coupled receptors, ATP-sensitive K+channels (Kir6.x) are tightly linked to cellular metabolism, and K+transport channels (Kir1.x, Kir4.x, Kir5.x, and Kir7.x). Inward rectification results from pore block by intracellular substances such as Mg2+and polyamines. Kir channel activity can be modulated by ions, phospholipids, and binding proteins. The basic building block of a Kir channel is made up of two transmembrane helices with cytoplasmic NH2and COOH termini and an extracellular loop which folds back to form the pore-lining ion selectivity filter. In vivo, functional Kir channels are composed of four such subunits which are either homo- or heterotetramers. Gene targeting and genetic analysis have linked Kir channel dysfunction to diverse pathologies. The crystal structure of different Kir channels is opening the way to understanding the structure-function relationships of this simple but diverse ion channel family.
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Walsh, Kenneth B. "Screening Technologies for Inward Rectifier Potassium Channels: Discovery of New Blockers and Activators." SLAS DISCOVERY: Advancing the Science of Drug Discovery 25, no. 5 (2020): 420–33. http://dx.doi.org/10.1177/2472555220905558.

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K+ channels play a critical role in maintaining the normal electrical activity of excitable cells by setting the cell resting membrane potential and by determining the shape and duration of the action potential. In nonexcitable cells, K+ channels establish electrochemical gradients necessary for maintaining salt and volume homeostasis of body fluids. Inward rectifier K+ (Kir) channels typically conduct larger inward currents than outward currents, resulting in an inwardly rectifying current versus voltage relationship. This property of inward rectification results from the voltage-dependent block of the channels by intracellular polyvalent cations and makes these channels uniquely designed for maintaining the resting potential near the K+ equilibrium potential (EK). The Kir family of channels consist of seven subfamilies of channels (Kir1.x through Kir7.x) that include the classic inward rectifier (Kir2.x) channel, the G-protein-gated inward rectifier K+ (GIRK) (Kir3.x), and the adenosine triphosphate (ATP)-sensitive (KATP) (Kir 6.x) channels as well as the renal Kir1.1 (ROMK), Kir4.1, and Kir7.1 channels. These channels not only function to regulate electrical/electrolyte transport activity, but also serve as effector molecules for G-protein-coupled receptors (GPCRs) and as molecular sensors for cell metabolism. Of significance, Kir channels represent promising pharmacological targets for treating a number of clinical conditions, including cardiac arrhythmias, anxiety, chronic pain, and hypertension. This review provides a brief background on the structure, function, and pharmacology of Kir channels and then focuses on describing and evaluating current high-throughput screening (HTS) technologies, such as membrane potential-sensitive fluorescent dye assays, ion flux measurements, and automated patch clamp systems used for Kir channel drug discovery.
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Xie, Lai-Hua, Scott A. John, Bernard Ribalet, and James N. Weiss. "Long Polyamines Act as Cofactors in PIP2 Activation of Inward Rectifier Potassium (Kir2.1) Channels." Journal of General Physiology 126, no. 6 (2005): 541–49. http://dx.doi.org/10.1085/jgp.200509380.

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Phosphatidylinosital-4,5-bisphosphate (PIP2) acts as an essential factor regulating the activity of all Kir channels. In most Kir members, the dependence on PIP2 is modulated by other factors, such as protein kinases (in Kir1), Gβγ (in Kir3), and the sulfonylurea receptor (in Kir6). So far, however, no regulator has been identified in Kir2 channels. Here we show that polyamines, which cause inward rectification by selectively blocking outward current, also regulate the interaction of PIP2 with Kir2.1 channels to maintain channel availability. Using spermine and diamines as polyamine analogs, we demonstrate that both spontaneous and PIP2 antibody–induced rundown of Kir2.1 channels in excised inside-out patches was markedly slowed by long polyamines; in contrast, polyamines with shorter chain length were ineffective. In K188Q mutant channels, which have a low PIP2 affinity, application PIP2 (10 μM) was unable to activate channel activity in the absence of polyamines, but markedly activated channels in the presence of long diamines. Using neomycin as a measure of PIP2 affinity, we found that long polyamines were capable of strengthening either the wild type or K188Q channels' interaction with PIP2. The negatively charged D172 residue inside the transmembrane pore region was critical for the shift of channel–PIP2 binding affinity by long polyamines. Sustained pore block by polyamines was neither sufficient nor necessary for this effect. We conclude that long polyamines serve a dual role as both blockers and coactivators (with PIP2) of Kir2.1 channels.
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Weaver, C. David, and Jerod S. Denton. "Next-generation inward rectifier potassium channel modulators: discovery and molecular pharmacology." American Journal of Physiology-Cell Physiology 320, no. 6 (2021): C1125—C1140. http://dx.doi.org/10.1152/ajpcell.00548.2020.

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Inward rectifying potassium (Kir) channels play important roles in both excitable and nonexcitable cells of various organ systems and could represent valuable new drug targets for cardiovascular, metabolic, immune, and neurological diseases. In nonexcitable epithelial cells of the kidney tubule, for example, Kir1.1 ( KCNJ1) and Kir4.1 ( KCNJ10) are linked to sodium reabsorption in the thick ascending limb of Henle’s loop and distal convoluted tubule, respectively, and have been explored as novel-mechanism diuretic targets for managing hypertension and edema. G protein-coupled Kir channels (Kir3) channels expressed in the central nervous system are critical effectors of numerous signal transduction pathways underlying analgesia, addiction, and respiratory-depressive effects of opioids. The historical dearth of pharmacological tool compounds for exploring the therapeutic potential of Kir channels has led to a molecular target-based approach using high-throughput screen (HTS) of small-molecule libraries and medicinal chemistry to develop “next-generation” Kir channel modulators that are both potent and specific for their targets. In this article, we review recent efforts focused specifically on discovery and improvement of target-selective molecular probes. The reader is introduced to fluorescence-based thallium flux assays that have enabled much of this work and then provided with an overview of progress made toward developing modulators of Kir1.1 (VU590, VU591), Kir2.x (ML133), Kir3.X (ML297, GAT1508, GiGA1, VU059331), Kir4.1 (VU0134992), and Kir7.1 (ML418). We discuss what is known about the small molecules’ molecular mechanisms of action, in vitro and in vivo pharmacology, and then close with our view of what critical work remains to be done.
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Troncoso Brindeiro, Carmen M., Rachel W. Fallet, Pascale H. Lane, and Pamela K. Carmines. "Potassium channel contributions to afferent arteriolar tone in normal and diabetic rat kidney." American Journal of Physiology-Renal Physiology 295, no. 1 (2008): F171—F178. http://dx.doi.org/10.1152/ajprenal.00563.2007.

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We previously reported an enhanced tonic dilator impact of ATP-sensitive K+ channels in afferent arterioles of rats with streptozotocin (STZ)-induced diabetes. The present study explored the hypothesis that other types of K+ channel also contribute to afferent arteriolar dilation in STZ rats. The in vitro blood-perfused juxtamedullary nephron technique was utilized to quantify afferent arteriolar lumen diameter responses to K+ channel blockers: 0.1–3.0 mM 4-aminopyridine (4-AP; KV channels), 10–100 μM barium (KIR channels), 1–100 nM tertiapin-Q (TPQ; Kir1.1 and Kir3.x subfamilies of KIR channels), 100 nM apamin (SKCa channels), and 1 mM tetraethylammonium (TEA; BKCa channels). In kidneys from normal rats, 4-AP, TEA, and Ba2+ reduced afferent diameter by 23 ± 3, 8 ± 4, and 18 ± 2%, respectively, at the highest concentrations employed. Neither TPQ nor apamin significantly altered afferent diameter. In arterioles from STZ rats, a constrictor response to TPQ (22 ± 4% decrease in diameter) emerged, and the response to Ba2+ was exaggerated (28 ± 5% decrease in diameter). Responses to the other K+ channel blockers were similar to those observed in normal rats. Moreover, exposure to either TPQ or Ba2+ reversed the afferent arteriolar dilation characteristic of STZ rats. Acute surgical papillectomy did not alter the response to TPQ in arterioles from normal or STZ rats. We conclude that 1) KV, KIR, and BKCa channels tonically influence normal afferent arteriolar tone, 2) KIR channels (including Kir1.1 and/or Kir3.x) contribute to the afferent arteriolar dilation during diabetes, and 3) the dilator impact of Kir1.1/Kir3.x channels during diabetes is independent of solute delivery to the macula densa.
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Cha, Tae-Joon, Joachim R. Ehrlich, Denis Chartier, Xiao-Yan Qi, Ling Xiao, and Stanley Nattel. "Kir3-Based Inward Rectifier Potassium Current." Circulation 113, no. 14 (2006): 1730–37. http://dx.doi.org/10.1161/circulationaha.105.561738.

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Le, Robert Q., Prathima Anandi, Xin Tian, et al. "Comparison of Donor KIR Genotype, Recipient CMV Reactivation and Pretransplant MRD in Predicting Relapse after Ex Vivo T-Deplete Allohsct." Blood 126, no. 23 (2015): 3212. http://dx.doi.org/10.1182/blood.v126.23.3212.3212.

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Abstract INTRODUCTION: Relapse is the most important cause of post-transplant mortality. The interaction between killer immunoglobulin-like receptors (KIRs) of donor natural killer (NK) cells and human leukocyte antigen (HLA)-class I molecules on recipient target cells may influence the outcome of allogeneic hematopoietic stem cell transplantation (HCT) by modulating NK cell alloreactivity. In addition to modulation by KIRs, NK cells also respond to CMV reactivation post-HCT to promote maturation and functional competence that could enhance their antileukemic effect. Since NK cells are postulated to play a prominent role in the setting of ex vivo T cell depleted HCT, we studied the relative contributions of KIR-mediated alloresponse and early CMV reactivation, in addition to measurable residual disease (MRD) status, on clinical outcomes. METHODS: A cohort of 109 consecutive patients who received myeloablative, HLA-identical sibling allogeneic peripheral blood HCT for hematological malignancies was studied at a single institution. All patients received a myeloablative preparative regimen (fludarabine 125 mg/m2, cyclophosphamide 120mg/kg, total body irradiation 400-1200 cGy based on age) followed by the infusion of a CD34+ selected graft from an HLA-identical sibling. Three models of donor KIRs were evaluated: a) KIR2DS1 positive (Venstrom, et al. NEJM 2012) seen in 41% of donors, b) "KIR3" - all 3 KIRs 2DL5A, 2DS1, and 3DS1 (Stringaris, et al. BBMT 2010) seen in 34% or, c) any KIR B genotype defining loci (KIR2DL5, 2DS1, 2DS2, 2DS3, 2DS5, or 3DS1) seen in 68%. CMV reactivation (65%) was described as a time-dependent covariate as well as dichotomized into early (< Day 60) vs other. Baseline multigene array MRD status was determined by RT-PCR (Goswami, et al. BMT 2015) and found to be positive in 6/21 (29%) of AML patients. Cox proportional hazards models were used. The cumulative incidence of relapse (CIR) was estimated and compared by the Gray's method to account for competing risks. RESULTS: Median recipient age was 43 years and median HCT-CI score was 3 (range 2 - 4). 40% of the cohort had AML, 26% ALL, 19% MDS, 10% NHL/CLL and 5% CML. At a median follow up of ~ 5 years, cumulative incidence of relapse was 35.4%, overall survival (OS) was 48.3% (95% CI 39.2-59.5), and NRM was 26.5%. CMV reactivation was not significantly associated with CIR as a time-dependent covariate (HR 1.4, P =0.35) or as a dichotomized covariate (HR 1.7, P =0. 16). Donor KIR2DS1 (HR 1.8, P = 0.07), KIR3 positivity (HR 1.9, P =0.06), and any haplotype B (HR 1.5, P =0.25) were not significantly associated with CIR. In the multivariate models adjusted for age at HCT, disease risk and CMV reactivation. However, MRD status in AML subjects was highly predictive of future relapse (MRD+ CIR was 83% vs MRD- CIR 21%, HR 7.5, p = 0.0015)(Figure 1). CONCLUSIONS: Pretransplant MRD (confined to AML subjects) strongly predicted future AML relapse in our models, and there was no significant association found with early CMV reactivation or with donor KIRs. Figure 1. Cumulative Incidence of Relapse by MRD Status. Figure 1. Cumulative Incidence of Relapse by MRD Status. Disclosures No relevant conflicts of interest to declare.
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Keselman, Inna, Miguel Fribourg, Dan P. Felsenfeld, and Diomedes E. Logothetis. "Mechanism of PLC-Mediated Kir3 Current Inhibition." Channels 1, no. 2 (2007): 113–23. http://dx.doi.org/10.4161/chan.4321.

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Zylbergold, Peter, and Terence E. Hébert. "Kir3 channel signalling complexes in cardiac arrhythmias." Drug Discovery Today: Disease Models 9, no. 3 (2012): e97-e102. http://dx.doi.org/10.1016/j.ddmod.2012.02.009.

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Bukiya, Anna N., and Avia Rosenhouse-Dantsker. "Modulation of Neuronal Kir3 Channels by Cholesterol." Biophysical Journal 110, no. 3 (2016): 608a. http://dx.doi.org/10.1016/j.bpj.2015.11.3245.

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Dissertations / Theses on the topic "Kir3"

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Todorov, Zlatomir. "Computational study of the structure-function relationship of Kir3 channels and applications to the design of light-gated Kir3 channels." Thesis, Université Grenoble Alpes (ComUE), 2019. http://www.theses.fr/2019GREAV030.

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Cette thèse de doctorat porte sur une famille de protéines transmembranaires exprimées sous forme de tétramères qui fonctionnent en tant que canaux ioniques sélectifs pour le potassium - le membre 3 des canaux potassiques à rectification entrante (Kir3). Quatre gènes codant pour les protéines Kir3 sont présents chez les mammifères dans la sous-famille, à savoir les membres Kir3.1-4. L'activité et l'expression tissulaire varient fortement en fonction des sous-unités constituant les canaux Kir3. Ces canaux sont activés par des interactions simultanées et directes avec des dimères bêta-gamma de la protéine G (Gβγ) libérés par les hétérotrimères de la protéine G de la classe G(i/o), des lipides PIP2 du feuillet interne de la membrane et des ions Na+ intracellulaires. Ces canaux permettent la genèse d’un courant potassique hyperpolarisant à des potentiels membranaires proches de l'EK. Ils jouent un rôle important dans la régulation de l'excitabilité cellulaire dans différents tissus. Des maladies ont été associées à une mauvaise régulation des canaux Kir3 de type sauvage ou à des mutations de leurs gènes.Un de mes objectifs a été de caractériser la dynamique conformationnelle sous-jacente à la fonction du canal Kir3.2 en utilisant la dynamique moléculaire. En partant de modèles obtenus par cristallographie aux rayons X, au lieu d’utiliser Gβγ pour ouvrir le canal dans nos simulations nous avons cherché à établir la stoichiométrie d’un ensemble de petites molécules connues pour l’activation de Kir3.2. Ainsi, dans une série de trajectoires où différentes combinaisons de partenaires étaient modélisées, le canal Kir3.2 a traversé différents états conformationnels et conducteurs – tout en reproduisant des caractéristiques décrites dans la littérature. Cette approche a amené à la découverte de nouveaux sites d'interaction lipide-protéine, potentiellement impliqués dans un mécanisme de rétroaction négative intrinsèque au canal Kir3.2. Cette prédiction est corroborée par des données de cristallographie aux rayons X publiées antérieurement et non exploitées dans ce contexte. L’analyse des trajectoires a également montré de nouvelles voies allostériques reliant les sites d’interaction du ligand aux portes du canal. De plus, sur la base de la dynamique du canal de type sauvage, nous avons proposé des mécanismes moléculaires pour plusieurs mutants pathologiques caractérisés expérimentalement.Parallèlement au projet théorique, j’ai travaillé à l’élaboration de canaux Kir3 sensibles à la lumière pour l’optogénétique. L’utilisation de modèles par homologie a guidé la sélection de résidus du canal qui ont été mutés en cystéine. La présence de cystéines réduites est nécessaire pour le marquage des protéines exprimées dans la membrane des ovocytes de Xenopus laevis avec les ligands photosensibles que nous avons utilisés. Parmi les vingt mutants cystéines criblées, l’un d’entre eux a montré un phénotype modéré de photo-activation. Ce phénotype a pu être considérablement amélioré par une mutation additionnelle, nous permettant d’obtenir le premier canal Kir3 constitutivement inactif et activable par la lumière.La procédure de simulation éprouvée dans ce travail est particulièrement adaptée à l’étude de divers canaux Kir3 d’intérêt. Une perspective pour nos modèles serait leur utilisation dans la conception de composés visant des conformations spécifiques du canal Kir3.2 en l’absence de données expérimentales sur les états d’ouverture et de fermeture complètes. Enfin, le canal Kir3.4 photosensible pourrait trouver des applications en biologie synthétique en tant que diode contrôlée par la lumière. En outre, ce mutant pourrait être inoculé in vivo – il devrait rester silencieux après marquage et fournir des informations sur le rôle physiologique de l'augmentation des courants médiés par canaux Kir3 lorsqu'il est activé par la lumière ultraviolette<br>This doctoral thesis focuses on a family of transmembrane proteins expressed as tetrameric assemblies which function as selective potassium ion channels – the potassium inward rectifier member 3 (Kir3). In the sub-family, four genes coding Kir3 proteins are present in mammals, namely, members Kir3.1 4. The activity and tissue-specific expression of Kir3 channels greatly vary with subunit composition. Kir3 channels are activated by direct simultaneous interactions with G-protein beta-gamma dimers (Gβγ) released from G-protein heterotrimers of the G(i/o) class, PIP2 lipids from the inner membrane leaflet and intracellular Na+ ions. These channels mediate hyperpolarizing potassium currents at membrane potentials close to EK, thus they are critical for development and health as they play an important role in decreasing cell excitability in different tissues. Disease conditions have been linked to misregulation of wild-type Kir3 channels or mutations of their genes.Starting from an X-ray crystallographic model, our goal was to obtain trajectories demonstrating simulated molecular dynamics of the wild-type Kir3.2 channel. We optimized a computational protocol using a set of brute-force simulations where different combinations of Kir3 activators were implemented. We observed the Kir3.2 channel transitioning between different conformational and conductive states – successfully reproducing dynamic features reported in the literature. We discovered novel functional lipid-protein interaction sites potentially involved in a negative-auto-feedback mechanism intrinsic to the Kir3.2 channel. Interestingly, this prediction is backed by previously published X ray crystallography data not exploited in this scope. Detailed analysis of the trajectories provided description of novel allosteric pathways linking the channel gates and the ligand interaction sites. In addition, based on the observed dynamics of the wild-type channel, we proposed molecular mechanisms for several experimentally-characterized pathologic mutants.In parallel to the computational project, we attempted to engineer light-gated Kir3 channels. This work was aided by homology models which guided the selection of positions satisfying an arbitrary set of criteria for cysteine mutagenesis. The presence of reduced cysteines is required for the labeling of the proteins expressed into the membrane of Xenopus laevis oocytes with the photoswitchable tethered ligands (PTL) we used. Among the twenty screened cysteine mutants, one construct showed a mild photo-blocking phenotype. Further engineering greatly improved this phenotype, yielding the first light-activated Kir3.4 homotetrameric channel.We believe that our simulation procedure is particularly suited for the investigation of various Kir3 assemblies of interest. An additional perspective for our models is to be used for the rational design of compounds targeting a specific conformation of Kir3.2 channel in the absence of experimentally obtained fully open/closed and transition-states conformations. Lastly, the developed photo-blocked Kir3.4 homotetramer could find applications in synthetic biology as a light-enabled diode. Alternatively, this mutant could be knocked-in in vivo – it should remain silent upon PTL-labeling in the resting-state, and provide information on the physiological role of the increase of Kir3 mediated currents when activated by ultra-violet light
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Rogalski, Sherri Lynn. "Modulation of Kir3 by lipids and tyrosine phosphorylation /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/6274.

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Ramakrishnan, Nitya. "Characterizing the roles of multiple Gbetagamma binding sites on Kir3 channels." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:8881/R/?func=dbin-jump-full&object_id=92394.

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Althof, Daniel [Verfasser], and Michael [Akademischer Betreuer] Frotscher. "Differential distribution of GABAB receptors, Kir3 and Cav2 ion channels in hippocampal parvalbumin and cholecystokinin expressing interneurons = Differenzielle Verteilung von GABAB Rezeptoren, Kir3 und Cav2 Ionenkanälen in Parvalbumin und Cholecystokinin exprimierenden Interneuronen des Hippocampus." Freiburg : Universität, 2012. http://d-nb.info/1115490699/34.

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Eulitz, Dirk. "Dopaminerge Neurone im motorischen und limbischen Mesencephalon der Ratte unterscheiden sich in ihrer Ausstattung mit Kir3-Kanälen." [S.l. : s.n.], 2000. http://www.diss.fu-berlin.de/2001/41/index.html.

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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 C can phosphorylate and inhibit Kir3 channels, yet the mechanism of inhibition and phosphorylation sites are incompletely understood. We took a combined experimental and computational approach using neuronal Kir3.2 to investigate how phosphorylation at a putative PKC site identified in Kir3.1/3.4 could lead to channel inhibition. Kir3.2 inhibition was found to depend on the phosphorylation state of Ser-196, although mutagenesis data suggest it functions as an allosteric regulator of PKC inhibition. MD simulations identified a molecular switch whereby phosphorylation of Ser-196 recruits a critical gating residue, Arg-201, away from the sodium coordination site Asp-228. Neutralization of Ser-196 or Arg-201 resulted in less active channels which exhibited increased sensitivity to PKC inhibition. Additionally the interplay of PIP2 and PKC inhibition was examined in depth using homomeric Kir3.2, revealing that increases in channel-PIP2 interactions limit sensitivity to PKC inhibition, whereas low levels of PIP2 increase PKC sensitivity. Neutralization of Ser-196 uncoupled PKC inhibition from this PIP2 dependence. These studies suggest a model whereby PKC inhibition can occur along PIP2-dependent and PIP2-independent pathways, depending on the phosphorylation state of Ser-196.
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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 theirfunctional properties. I originally described the differential modulatory effects oftwo RGS proteins, the RGS3 short isoform (RGS3s) and RGS4, on muscarinicm2 and serotonin 1A receptor-coupled Kir3.1/Kir3.2a channels expressed inChinese hamster ovary (CHO-K1) cells. Both RGS3s and RGS4 acceleratedGIRK activation and deactivation current kinetics in a similar way. However, onlyRGS3s si gnificantly decreased the maximal GIRK current (Imax) elicited by ACh(~45% inhibition) and significantly increased the EC50 for both GPCRs. Thehypothesis that emerged from this initial study was that the distinct RGS4 Nterminaldomain mediated a direct coupling of RGS4 to GPCR-GIRK channelsignaling complexes that was not shared by RGS3s. To test this hypothesis, Iepitope-tagged several GPCRs, the Kir3.1 subunit, RGS3s, RGS4, and severaldeletion mutants and chimeras for co-immunoprecipitation experiments. Using anepitope-tagged degradation resistant RGS4 mutant RGS4(C2V), I detected coprecipitationof different GPCR-GIRK channel complexes with RGS4 but notRGS3s.The functional impact of RGS4 coupling to the GPCR-Kir3 channelcomplex versus uncoupled RGS3s was not apparent in recordings from CHO-K1cells presumably due to a high degree of RGS collision-coupling. Controlledexpression in Xenopus oocytes revealed a 30-fold greater potency for RGS4 inthe accelerating GIRK channel gating kinetics. In summary, these findings demonstrate that one of the ways for the cellto achieve signaling pathway specificity may be through selective coupling of thedifferent GPCR-effector-RGS protein complexes.
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Alexander, Agathe Katharina [Verfasser], Lutz [Gutachter] Pott, and Bodo Kornelius Hubertus [Gutachter] Brandts. "Untersuchungen zur Regulation von Kir3-Kanälen in atrialen Myozyten durch Phosphatidylinositol-4,5-bisphosphat mit Hilfe der spannungsabhängigen Phosphatase Ciona intestinalis – voltage sensor containing phosphatase (Ci – VSP) / Agathe Katharina Alexander. Gutachter: Lutz Pott ; Bodo Kornelius Hubertus Brandts." Bochum : Ruhr-Universität Bochum, 2016. http://d-nb.info/1105035980/34.

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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 specific reciprocal residue interactions between the two proteins are currently known. Given the absence of direct structural evidence, we attempted to identify these functionally important channel-Gβγ interactions using a computational approach. We developed a multistage computational docking algorithm that combines several known methods in protein-protein docking. Application of the docking protocol to previously published structures of Gβγ and GIRK1 homomeric channels produced a clear signal of a favored binding mode. Analysis of this binding mode suggested a mechanism by which Gβγ promotes the open state of the channel. The channel-Gβγ interactions predicted by the model in silico could be disrupted in vitro by mutation of one protein and rescued by additional mutation of reciprocal residues in the other protein. These interactions were found to extend to agonist induced activation of the channels as well as to activation of the native heteromeric channels. Currently, the structural mechanism by which Gβγ regulates the functional conformations of GIRK channels or of any of its membrane-associated effector proteins is not known. This work shows the first evidence for specific reciprocal interactions between Gβγ and a GIRK channel and places these interactions in the context of a general model of intracellular regulation of GIRK gating.
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Tromp, Anna Kira [Verfasser]. "Multipartikuläre Minitabletten / Anna Kira Tromp." München : Verlag Dr. Hut, 2020. http://d-nb.info/1219475068/34.

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Books on the topic "Kir3"

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Kira-kira. Thorndike Press, 2005.

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Kira-Kira. Atheneum Books for Young Readers, 2004.

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Kira-kira. Atheneum Books for Young Readers, 2004.

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Kira-Kira. Aladdin, 2005.

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Kadohata, Cynthia. Kira-kira. NXB Trẻ, 2005.

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1970-, Şik Ahmet, ed. Kirk katir kirk satir. İthaki, 2010.

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Özel, Sevgi. Dil kiri el kiri. Bilgi Yayınevi, 2000.

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Llorente, David. Kira. Zócalo Editorial, 1998.

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Kirk Douglas. St. Martin's Press, 1985.

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Petrovski, Trajan. Vovčeto Kiro. Detska radost, 1988.

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Book chapters on the topic "Kir3"

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Seitz, Viola, Philip Stötzner, Dominika Labuz, and Halina Machelska. "Patch Clamp Analysis of Opioid-Induced Kir3 Currents in Mouse Peripheral Sensory Neurons Following Nerve Injury." In Methods in Molecular Biology. Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0884-5_12.

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Gooch, Jan W. "Kira-ye." In Encyclopedic Dictionary of Polymers. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_6676.

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Gutierrez, Sebastian. "Kira Radinsky." In Data Scientists at Work. Apress, 2014. http://dx.doi.org/10.1007/978-1-4302-6599-3_14.

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Scruton, Roger. "Russell Kirk." In Conservative Texts. Palgrave Macmillan UK, 1991. http://dx.doi.org/10.1007/978-1-349-21728-1_11.

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Whyte, Ian D. "Kirk and Culture." In Scotland’s Society and Economy in Transition, c.1500–c.1760. Macmillan Education UK, 1997. http://dx.doi.org/10.1007/978-1-349-25307-4_4.

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Hoff, Karin. "Kirk, Hans Rudolf." In Kindlers Literatur Lexikon (KLL). J.B. Metzler, 2020. http://dx.doi.org/10.1007/978-3-476-05728-0_10449-1.

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Kossovsky, Nir. "Avoiding Hara-Kiri." In Reputation, Stock Price, and You. Apress, 2012. http://dx.doi.org/10.1007/978-1-4302-4891-0_1.

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Anatol, Giselle Liza. "Ghosts of Japanese/American History in Kira-Kira (2005)." In Dust Off the Gold Medal. Routledge, 2021. http://dx.doi.org/10.4324/9780367337223-13-14.

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Alstrup, Kaj, and KLL. "Kirk, Hans Rudolf: Fiskerne." In Kindlers Literatur Lexikon (KLL). J.B. Metzler, 2020. http://dx.doi.org/10.1007/978-3-476-05728-0_10450-1.

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Thomas, R. Roosevelt. "Die Pionier-Giraffe: Kirk." In Management of Diversity. Gabler Verlag, 2001. http://dx.doi.org/10.1007/978-3-322-84445-3_13.

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Conference papers on the topic "Kir3"

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Zuckerman, Oren, Guy Hoffman, Daphne Kopelman-Rubin, et al. "KIP3." In TEI '16: Tenth International Conference on Tangible, Embedded, and Embodied Interaction. ACM, 2016. http://dx.doi.org/10.1145/2839462.2856535.

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Cohen, Jonathan. "“Kirk here:”." In INTERACT '93 and CHI '93 conference companion. ACM Press, 1993. http://dx.doi.org/10.1145/259964.260073.

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Chan, Daniel C. F., Zhiyong Zhang, Hong Wang, et al. "Abstract 3656: Therapeutic effects of anti-KIR antibodies against metastatic cancer cells with aberrant expression of Natural Killer-Cell Immunoglobulin-like Receptors (KIRs)." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3656.

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"In Memoriam - Joseph Kirk Armintor." In IEEE Industry Applications Society 51st Annual Petroleum and Chemical Industry Conference. IEEE, 2004. http://dx.doi.org/10.1109/pcicon.2004.1352755.

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"In memoriam - J. Kirk Armintor." In Conference Record of 2004 Annual Pulp and Paper Industry Technical Conference. IEEE, 2004. http://dx.doi.org/10.1109/papcon.2004.1338349.

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Mosawi, Aamir Al. "P504 Sanjad-sakati-richardson-kirk syndrome." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.840.

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Kasnowihardjo, Gunadi. ""MELACAK JEJAK BUDAYA AUSTRONESIA DI KAWASAN PANTURA P. MADURA PADA MASA PRASEJARAH – PROTOSEJARAH "." In Seminar Nasional Arkeologi 2019. Balai Arkeologi Jawa Barat, 2020. http://dx.doi.org/10.24164/prosiding.v3i1.3.

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Terinspirasi oleh teori “Out of Taiwan” atau “Express Train Hypothesis”, bahwa imigran penutur bahasa Austronesia mencapai Pulau Jawa kira-kira 500 BC. Melacak jejak budaya Austronesia di kawasan pantai utara Pulau Madura ini adalah penelitian lanjutan dari tema penelitian “Melacak Jejak – Jejak Budaya Austronesia di Kawasan Pantai Utara Jawa”. Dalam pelacakan jejak budaya Austronesia digunakan tiga kajian yaitu Geomorfologi, Arkeologi, dan Etnografi yang dilakukan dengan kegiatan lapangan yaitu survey dan ekskavasi. Sedangkan kegiatan pasca lapangan antara lain analisis laboratorium yang hasilnya sebagai data pendukung dalam interpretasi.
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Erbe, Amy K., Wei Wang, Lakeesha Carmichael, et al. "Abstract LB-048: Impact of KIR/KIR ligand genotype for neuroblastoma patients in a Phase 3 COG immunotherapy trial." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-048.

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Amato, Flora, Vincenzo Moscato, Antonio Picariello, and Giancarlo Sperli. "KIRA: A System for Knowledge-Based Access to Multimedia Art Collections." In 2017 IEEE 11th International Conference on Semantic Computing (ICSC). IEEE, 2017. http://dx.doi.org/10.1109/icsc.2017.59.

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Jiang, Hao, Jie Zheng, and Marco Racanelli. "Kirk Effect Induced Bias Dependency of Thermal Resistance in SiGe HBTs." In 2008 IEEE Topical Meeting on Silicon Monolithic Integrated Circuits in RF Systems. IEEE, 2008. http://dx.doi.org/10.1109/smic.2008.25.

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Reports on the topic "Kir3"

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Varbanova, Viktoria, Snejina Mihailova, Elissaveta Naumova, and Anastasiya Mihaylova. Distribution of Killer-cell Immunoglobulin-like Receptors (KIR) and their HLA Class I Ligands in the Bulgarian Population. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, 2020. http://dx.doi.org/10.7546/crabs.2020.07.14.

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Ceylan, Mustafa. Toplumun Faizli Krediye Dair Değişen Algısı Hakkında Bir Mülakat Çalışması. İLKE İlim Kültür Eğitim Vakfı, 2021. http://dx.doi.org/10.26414/ikm004.

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Faiz, en bilinen tabiri ile kiralanan paranın kira bedeli anlamındadır. İslam iktisadı, Bakara Suresi’nin 275 ayeti kerimesinde de bildirildiği üzere ticaretin helal, faizin (ribâ) haram kılınması düsturu ile hareket etmektedir. Bu çalışmanın amacı, yukarıda bahsedilen faizin haramlığı düsturu da temel alınarak, günümüz kapitalist sisteminde kilit rol oynayan faizin, bireylerin bakış açılarında nasıl bir yer edindiğini araştırmak için yapılmıştır. İslam iktisadının ilkelerini yerine getirmeye çalışılarak oluşturulan kurumların, toplum tarafından nasıl değerlendirildiği de öğrenilmiş olunacaktır. Çalışma boyunca nitel araştırma yöntemi kullanılmıştır. Nitel araştırmada veri toplamak için mülakat yöntemi tercih edilmiştir. Mülakata katılan kişi sayısı 23 kişi olarak belirlenmiştir. Temel bulgulara göre, mülakatlara katılan bireylerin çoğu çevreden borç istemeden bankalara gitmektedir. Toplumsal ilişkilerin, maddi konularda yeterince kapsayıcı olmadığı göze çarpmaktadır. Bununla birlikte bireyler kendi yuvalarını kurmak için yuvadan ayrıldıkları zaman kendi ailelerine karşı “el(yabancı)” statüsüne geçmektedirler. Araştırmamız için görüştüğümüz bireylerden, ihtiyacı olan maddi miktarı bulmanın yollarından biri olan alternatif kurumları bilen birey sayısının az olduğu tespit edilmiştir. Tekrar faizli kredi çekmeyi düşünen bireylerin bu kararlarındaki en önemli etken “hayallerini ertelememek üzerine kurulu bir dünya görüşüne” sahip olmalarıdır.
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