ML297 (VU0456810), the first potent and selective activator of the GIRK potassium channel, displays antiepileptic properties in mice.
暂无分享,去创建一个
B. Zou | C. Lindsley | G. Sliwoski | J. S. Daniels | Xinmin Xie | C. Niswender | Liya Yang | Emily L. Days | C. Weaver | Kristian Kaufmann | Ian M. Romaine | C. Pascual | Adam Malik | Yu Du | R. Morrison | J. Denton | G. Sulikowski | C. Weaver | J. Daniels | Gregory Sliwoski | X. Xie
[1] L. Bierut,et al. Family‐based genome‐wide association study of frontal theta oscillations identifies potassium channel gene KCNJ6 , 2012, Genes, brain, and behavior.
[2] Adam Malik,et al. Rodent motor and neuropsychological behaviour measured in home cages using the integrated modular platform SmartCage™ , 2012, Clinical and experimental pharmacology & physiology.
[3] S. Herzer,et al. G-protein-gated inwardly rectifying K+ channel 4 (GIRK4) immunoreactivity in chemically defined neurons of the hypothalamic arcuate nucleus that control body weight , 2012, Journal of Chemical Neuroanatomy.
[4] Kazuo Yamada,et al. Association study of the KCNJ3 gene as a susceptibility candidate for schizophrenia in the Chinese population , 2011, Human Genetics.
[5] J. Hanrahan,et al. Naringin directly activates inwardly rectifying potassium channels at an overlapping binding site to tertiapin‐Q , 2011, British journal of pharmacology.
[6] Maria-Christina Zennaro,et al. Mutations in KCNJ5 gene cause hyperaldosteronism. , 2011, Circulation research.
[7] J. Svendsen,et al. Common Polymorphisms in KNCJ5 Are Associated with Early-Onset Lone Atrial Fibrillation in Caucasians , 2011, Cardiology.
[8] K. Ikeda,et al. Identification of Selective Agonists and Antagonists to G Protein-Activated Inwardly Rectifying Potassium Channels: Candidate Medicines for Drug Dependence and Pain , 2011, Current neuropharmacology.
[9] Toru Yamashita,et al. Effects of a Highly Selective Acetylcholine-Activated K+ Channel Blocker on Experimental Atrial Fibrillation , 2011, Circulation. Arrhythmia and electrophysiology.
[10] Brian A. Chauder,et al. Small-molecule modulators of inward rectifier K+ channels: recent advances and future possibilities. , 2010, Future medicinal chemistry.
[11] C. Lüscher,et al. Emerging roles for G protein-gated inwardly rectifying potassium (GIRK) channels in health and disease , 2010, Nature Reviews Neuroscience.
[12] I. Sora,et al. Association between KCNJ6 (GIRK2) Gene Polymorphisms and Postoperative Analgesic Requirements after Major Abdominal Surgery , 2009, PloS one.
[13] Masahiko Watanabe,et al. Subcellular compartment‐specific molecular diversity of pre‐ and post‐synaptic GABAB‐activated GIRK channels in Purkinje cells , 2009, Journal of neurochemistry.
[14] R. Luján,et al. New sites of action for GIRK and SK channels , 2009, Nature Reviews Neuroscience.
[15] S. Choe,et al. A Discrete Alcohol Pocket Involved in GIRK Channel Activation , 2009, Nature Neuroscience.
[16] P. Visscher,et al. Family-based genome-wide association studies. , 2009, Pharmacogenomics.
[17] Kari A. Johnson,et al. A Novel Assay of Gi/o-Linked G Protein-Coupled Receptor Coupling to Potassium Channels Provides New Insights into the Pharmacology of the Group III Metabotropic Glutamate Receptors , 2008, Molecular Pharmacology.
[18] G. Peltz,et al. Quantitative trait locus and computational mapping identifies Kcnj9 (GIRK3) as a candidate gene affecting analgesia from multiple drug classes , 2008, Pharmacogenetics and genomics.
[19] Craig W Lindsley,et al. Application of combinatorial chemistry science on modern drug discovery. , 2008, Journal of combinatorial chemistry.
[20] C. Lüscher,et al. Bi-directional effects of GABAB receptor agonists on the mesolimbic dopamine system , 2004, Nature Neuroscience.
[21] H. Niki,et al. Ethanol opens G-protein-activated inwardly rectifying K+ channels , 1999, Nature Neuroscience.
[22] T. Maeda,et al. Characterization of G-Protein-Gated K+ Channels Composed of Kir3.2 Subunits in Dopaminergic Neurons of the Substantia Nigra , 1999, The Journal of Neuroscience.
[23] L. Jan,et al. Normal cerebellar development but susceptibility to seizures in mice lacking G protein-coupled, inwardly rectifying K+ channel GIRK2. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[24] D. Clapham,et al. Cloning of a Xenopus laevis Inwardly Rectifying K+ Channel Subunit That Permits GIRK1 Expression of IKACh Currents in Oocytes , 1996, Neuron.
[25] D. Clapham,et al. The G-protein-gated atrial K+ channel IKAch is a heteromultimer of two inwardly rectifying K+-channel proteins , 1995, Nature.
[26] M. Lazdunski,et al. Cloning provides evidence for a family of inward rectifier and G‐protein coupled K+ channels in the brain , 1994, FEBS letters.
[27] Y. Jan,et al. Activation of the cloned muscarinic potassium channel by G protein βγ subunits , 1994, Nature.
[28] D. Clapham,et al. Recombinant G-protein βγ-subunits activate the muscarinic-gated atrial potassium channel , 1994, Nature.
[29] R. Iyengar,et al. The G protein-gated atrial K+ channel is stimulated by three distinct GIα-subunits , 1988, Nature.
[30] D. Clapham,et al. The βγ subunits of GTP-binding proteins activate the muscarinic K+ channel in heart , 1987, Nature.
[31] Y. Jan,et al. Activation of the cloned muscarinic potassium channel by G protein beta gamma subunits. , 1994, Nature.
[32] D. Clapham,et al. Recombinant G-protein beta gamma-subunits activate the muscarinic-gated atrial potassium channel. , 1994, Nature.
[33] D. Clapham,et al. The beta gamma subunits of GTP-binding proteins activate the muscarinic K+ channel in heart. , 1987, Nature.