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Summary Expression Phenotypes Gene Literature (91) GO Terms (4) Nucleotides (85) Proteins (58) Interactants (104) Wiki
XB-GENEPAGE-5919505

Papers associated with kcnj5



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A revised mechanism of action of hyperaldosteronism-linked mutations in cytosolic domains of GIRK4 (KCNJ5)., Shalomov B, Handklo-Jamal R, Reddy HP, Theodor N, Bera AK, Dascal N., J Physiol. March 1, 2022; 600 (6): 1419-1437.


Consequences of somatic mutations of GIRK1 detected in primary malign tumors on expression and function of G-protein activated, inwardly rectifying, K+ channels., Pelzmann B, Hatab A, Scheruebel S, Langthaler S, Rienmueller T, Sokolowski A, Gorischek A, Platzer D, Zorn-Pauly K, Jahn SW, Bauernhofer T, Schreibmayer W., Front Oncol. January 1, 2022; 12 998907.


Identification of a unique endoplasmic retention motif in the Xenopus GIRK5 channel and its contribution to oocyte maturation., Rangel-Garcia CI, Salvador C, Chavez-Garcia K, Diaz-Bello B, Lopez-Gonzalez Z, Vazquez-Cruz L, Angel Vazquez-Martinez J, Ortiz-Navarrete V, Riveros-Rosas H, Escobar LI., FEBS Open Bio. April 1, 2021; 11 (4): 1093-1108.            


The small molecule GAT1508 activates brain-specific GIRK1/2 channel heteromers and facilitates conditioned fear extinction in rodents., Xu Y, Cantwell L, Molosh AI, Plant LD, Gazgalis D, Fitz SD, Dustrude ET, Yang Y, Kawano T, Garai S, Noujaim SF, Shekhar A, Logothetis DE, Thakur GA., J Biol Chem. March 13, 2020; 295 (11): 3614-3634.  


Mutant KCNJ3 and KCNJ5 Potassium Channels as Novel Molecular Targets in Bradyarrhythmias and Atrial Fibrillation., Yamada N, Asano Y, Fujita M, Yamazaki S, Inanobe A, Matsuura N, Kobayashi H, Ohno S, Ebana Y, Tsukamoto O, Ishino S, Takuwa A, Kioka H, Yamashita T, Hashimoto N, Zankov DP, Shimizu A, Asakura M, Asanuma H, Kato H, Nishida Y, Miyashita Y, Shinomiya H, Naiki N, Hayashi K, Makiyama T, Ogita H, Miura K, Ueshima H, Komuro I, Yamagishi M, Horie M, Kawakami K, Furukawa T, Koizumi A, Kurachi Y, Sakata Y, Minamino T, Kitakaze M, Takashima S., Circulation. April 30, 2019; 139 (18): 2157-2169.


Familial Sinus Node Disease Caused by a Gain of GIRK (G-Protein Activated Inwardly Rectifying K+ Channel) Channel Function., Kuß J, Stallmeyer B, Goldstein M, Rinné S, Pees C, Zumhagen S, Seebohm G, Decher N, Pott L, Kienitz MC, Schulze-Bahr E., Circ Genom Precis Med. January 1, 2019; 12 (1): e002238.


Ivermectin activates GIRK channels in a PIP2 -dependent, Gβγ -independent manner and an amino acid residue at the slide helix governs the activation., Chen IS, Tateyama M, Fukata Y, Uesugi M, Kubo Y., J Physiol. September 1, 2017; 595 (17): 5895-5912.


Novel Insertion Mutation in KCNJ5 Channel Produces Constitutive Aldosterone Release From H295R Cells., Hardege I, Xu S, Gordon RD, Thompson AJ, Figg N, Stowasser M, Murrell-Lagnado R, O'Shaughnessy KM., Mol Endocrinol. October 1, 2015; 29 (10): 1522-30.


Identification of the Intracellular Na+ Sensor in Slo2.1 Potassium Channels., Thomson SJ, Hansen A, Sanguinetti MC., J Biol Chem. June 5, 2015; 290 (23): 14528-35.


9B.03: A NOVEL INSERTIONAL SOMATIC KCNJ5 MUTATION IN AN AUSTRALIAN PATIENT WITH AN ALDOSTERONE PRODUCING ADENOMA., Xu S, Hardege I, Murthy M, Gordon R, Stowasser M, OʼShaughnessy K., J Hypertens. June 1, 2015; 33 Suppl 1 e120.


Cardiac arrhythmia induced by genetic silencing of 'funny' (f) channels is rescued by GIRK4 inactivation., Mesirca P, Alig J, Torrente AG, Müller JC, Marger L, Rollin A, Marquilly C, Vincent A, Dubel S, Bidaud I, Fernandez A, Seniuk A, Engeland B, Singh J, Miquerol L, Ehmke H, Eschenhagen T, Nargeot J, Wickman K, Isbrandt D, Mangoni ME., Nat Commun. August 21, 2014; 5 4664.                


Differential effects of genetically-encoded Gβγ scavengers on receptor-activated and basal Kir3.1/Kir3.4 channel current in rat atrial myocytes., Kienitz MC, Mintert-Jancke E, Hertel F, Pott L., Cell Signal. June 1, 2014; 26 (6): 1182-1192.


Role for germline mutations and a rare coding single nucleotide polymorphism within the KCNJ5 potassium channel in a large cohort of sporadic cases of primary aldosteronism., Murthy M, Xu S, Massimo G, Wolley M, Gordon RD, Stowasser M, O'Shaughnessy KM., Hypertension. April 1, 2014; 63 (4): 783-9.


A Kir3.4 mutation causes Andersen-Tawil syndrome by an inhibitory effect on Kir2.1., Kokunai Y, Nakata T, Furuta M, Sakata S, Kimura H, Aiba T, Yoshinaga M, Osaki Y, Nakamori M, Itoh H, Sato T, Kubota T, Kadota K, Shindo K, Mochizuki H, Shimizu W, Horie M, Okamura Y, Ohno K, Takahashi MP., Neurology. March 25, 2014; 82 (12): 1058-64.


RGS4 regulates partial agonism of the M2 muscarinic receptor-activated K+ currents., Chen IS, Furutani K, Inanobe A, Kurachi Y., J Physiol. March 15, 2014; 592 (6): 1237-48.            


Molecular basis of the facilitation of the heterooligomeric GIRK1/GIRK4 complex by cAMP dependent protein kinase., Treiber F, Rosker C, Keren-Raifman T, Steinecker B, Gorischek A, Dascal N, Schreibmayer W., Biochim Biophys Acta. April 1, 2013; 1828 (4): 1214-21.              


Characterization of a novel somatic KCNJ5 mutation delI157 in an aldosterone-producing adenoma., Murthy M, Azizan EA, Brown MJ, O'Shaughnessy KM., J Hypertens. September 1, 2012; 30 (9): 1827-33.


Crystal structure of the mammalian GIRK2 K+ channel and gating regulation by G proteins, PIP2, and sodium., Whorton MR, MacKinnon R., Cell. September 30, 2011; 147 (1): 199-208.


Inhibition of G protein-activated inwardly rectifying K+ channels by different classes of antidepressants., Kobayashi T, Washiyama K, Ikeda K., PLoS One. January 1, 2011; 6 (12): e28208.            


Cloning and characterisation of GIRK1 variants resulting from alternative RNA editing of the KCNJ3 gene transcript in a human breast cancer cell line., Wagner V, Stadelmeyer E, Riederer M, Regitnig P, Gorischek A, Devaney T, Schmidt K, Tritthart HA, Hirschberg K, Bauernhofer T, Schreibmayer W., J Cell Biochem. June 1, 2010; 110 (3): 598-608.


Heteromeric assembly of inward rectifier channel subunit Kir2.1 with Kir3.1 and with Kir3.4., Ishihara K, Yamamoto T, Kubo Y., Biochem Biophys Res Commun. March 20, 2009; 380 (4): 832-7.


Specificity of Gbetagamma signaling depends on Galpha subunit coupling with G-protein-sensitive K(+) channels., Geng X, Du XN, Rusinova R, Liu BY, Li F, Zhang X, Chen XJ, Logothetis DE, Zhang HL., Pharmacology. January 1, 2009; 84 (2): 82-90.


Subunit stoichiometry of heterologously expressed G-protein activated inwardly rectifying potassium channels analysed by fluorescence intensity ratio measurement., Grasser E, Steinecker B, Ahammer H, Schreibmayer W., Pflugers Arch. March 1, 2008; 455 (6): 1017-24.


Characterizations of a loss-of-function mutation in the Kir3.4 channel subunit., Calloe K, Ravn LS, Schmitt N, Sui JL, Duno M, Haunso S, Grunnet M, Svendsen JH, Olesen SP., Biochem Biophys Res Commun. December 28, 2007; 364 (4): 889-95.


Inhibition by cocaine of G protein-activated inwardly rectifying K+ channels expressed in Xenopus oocytes., Kobayashi T, Nishizawa D, Iwamura T, Ikeda K., Toxicol In Vitro. June 1, 2007; 21 (4): 656-64.


The GIRK1 brain variant GIRK1d and its functional impact on heteromultimeric GIRK channels., Steinecker B, Rosker C, Schreibmayer W., J Recept Signal Transduct Res. January 1, 2007; 27 (5-6): 369-82.


Base of pore loop is important for rectification, activation, permeation, and block of Kir3.1/Kir3.4., Makary SM, Claydon TW, Dibb KM, Boyett MR., Biophys J. June 1, 2006; 90 (11): 4018-34.


A difference in inward rectification and polyamine block and permeation between the Kir2.1 and Kir3.1/Kir3.4 K+ channels., Makary SM, Claydon TW, Enkvetchakul D, Nichols CG, Boyett MR., J Physiol. November 1, 2005; 568 (Pt 3): 749-66.


Mutation of critical GIRK subunit residues disrupts N- and C-termini association and channel function., Sarac R, Hou P, Hurley KM, Hriciste D, Cohen NA, Nelson DJ., J Neurosci. February 16, 2005; 25 (7): 1836-46.


RFamide-related peptides signal through the neuropeptide FF receptor and regulate pain-related responses in the rat., Pertovaara A, Ostergård M, Ankö ML, Lehti-Koivunen S, Brandt A, Hong W, Korpi ER, Panula P., Neuroscience. January 1, 2005; 134 (3): 1023-32.


K+ activation of kir3.1/kir3.4 and kv1.4 K+ channels is regulated by extracellular charges., Claydon TW, Makary SY, Dibb KM, Boyett MR., Biophys J. October 1, 2004; 87 (4): 2407-18.


Short variable sequence acquired in evolution enables selective inhibition of various inward-rectifier K+ channels., Ramu Y, Klem AM, Lu Z., Biochemistry. August 24, 2004; 43 (33): 10701-9.


Molecular determinants responsible for differential cellular distribution of G protein-gated inwardly rectifying K+ channels., Mirshahi T, Logothetis DE., J Biol Chem. March 19, 2004; 279 (12): 11890-7.


Mechanosensitivity of GIRK channels is mediated by protein kinase C-dependent channel-phosphatidylinositol 4,5-bisphosphate interaction., Zhang L, Lee JK, Lee JK, John SA, Uozumi N, Kodama I., J Biol Chem. February 20, 2004; 279 (8): 7037-47.


Molecular basis for the inhibition of G protein-coupled inward rectifier K(+) channels by protein kinase C., Mao J, Wang X, Chen F, Wang R, Rojas A, Shi Y, Piao H, Jiang C., Proc Natl Acad Sci U S A. January 27, 2004; 101 (4): 1087-92.


The selectivity filter may act as the agonist-activated gate in the G protein-activated Kir3.1/Kir3.4 K+ channel., Claydon TW, Makary SY, Dibb KM, Boyett MR., J Biol Chem. December 12, 2003; 278 (50): 50654-63.


Inhibition of G-protein-coupled inward rectifying K+ channels by intracellular acidosis., Mao J, Wu J, Chen F, Wang X, Jiang C., J Biol Chem. February 28, 2003; 278 (9): 7091-8.


Single channel analysis of the regulation of GIRK1/GIRK4 channels by protein phosphorylation., Müllner D., Biophys J. February 1, 2003; 84 (2 Pt 1): 1399-409.


Early embryonic expression of ion channels and pumps in chick and Xenopus development., Rutenberg J, Cheng SM, Levin M., Dev Dyn. December 1, 2002; 225 (4): 469-84.                            


Molecular determinants for activation of G-protein-coupled inward rectifier K+ (GIRK) channels by extracellular acidosis., Mao J, Li L, McManus M, Wu J, Cui N, Jiang C., J Biol Chem. November 29, 2002; 277 (48): 46166-71.


N-terminal tyrosine residues within the potassium channel Kir3 modulate GTPase activity of Galphai., Ippolito DL, Temkin PA, Rogalski SL, Chavkin C., J Biol Chem. September 6, 2002; 277 (36): 32692-6.


Functional expression of a novel ginsenoside Rf binding protein from rat brain mRNA in Xenopus laevis oocytes., Choi S, Jung SY, Ko YS, Koh SR, Rhim H, Nah SY., Mol Pharmacol. April 1, 2002; 61 (4): 928-35.


Gbeta residues that do not interact with Galpha underlie agonist-independent activity of K+ channels., Mirshahi T, Robillard L, Zhang H, Hébert TE, Logothetis DE., J Biol Chem. March 1, 2002; 277 (9): 7348-55.


G protein-gated inwardly rectifying potassium channels are targets for volatile anesthetics., Weigl LG, Schreibmayer W., Mol Pharmacol. August 1, 2001; 60 (2): 282-9.


Identification of G protein-coupled, inward rectifier potassium channel gene products from the rat anterior pituitary gland., Gregerson KA, Flagg TP, O'Neill TJ, Anderson M, Lauring O, Horel JS, Welling PA., Endocrinology. July 1, 2001; 142 (7): 2820-32.


Inhibition of a Gi-activated potassium channel (GIRK1/4) by the Gq-coupled m1 muscarinic acetylcholine receptor., Hill JJ, Peralta EG., J Biol Chem. February 23, 2001; 276 (8): 5505-10.


Residues and mechanisms for slow activation and Ba2+ block of the cardiac muscarinic K+ channel, Kir3.1/Kir3.4., Lancaster MK, Dibb KM, Quinn CC, Leach R, Lee JK, Lee JK, Findlay JB, Boyett MR., J Biol Chem. November 17, 2000; 275 (46): 35831-9.


Single channel studies of inward rectifier potassium channel regulation by muscarinic acetylcholine receptors., Bard J, Kunkel MT, Peralta EG., J Gen Physiol. November 1, 2000; 116 (5): 645-52.          


G-protein mediated gating of inward-rectifier K+ channels., Mark MD, Herlitze S., Eur J Biochem. October 1, 2000; 267 (19): 5830-6.


Cs+ block of the cardiac muscarinic K+ channel, GIRK1/GIRK4, is not dependent on the aspartate residue at position 173., Dibb KM, Leach R, Lancaster MK, Findlay JB, Boyett MR., Pflugers Arch. September 1, 2000; 440 (5): 740-4.

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