RGS8 accelerates G-protein-mediated modulation of K+currents

[1]  M. Koelle.  A new family of G-protein regulators - the RGS proteins. , 1997, Current opinion in cell biology.

[2]  R. Matsuda,et al.  Expression of neurofilament proteins in proliferating C2C12 mouse skeletal muscle cells. , 1996, Experimental cell research.

[3]  T. Wieland,et al.  RGS-r, a retinal specific RGS protein, binds an intermediate conformation of transducin and enhances recycling. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[4]  B. Bean,et al.  GABAB Receptor-Activated Inwardly Rectifying Potassium Current in Dissociated Hippocampal CA3 Neurons , 1996, The Journal of Neuroscience.

[5]  G. Westbrook,et al.  Metabotropic Glutamate Receptors Activate G-Protein-Coupled Inwardly Rectifying Potassium Channels in XenopusOocytes , 1996, The Journal of Neuroscience.

[6]  T. Hunt,et al.  RGS10 is a selective activator of Gαi GTPase activity , 1996, Nature.

[7]  K. Blumer,et al.  RGS family members: GTPase-activating proteins for heterotrimeric G-protein α-subunits , 1996, Nature.

[8]  A. Gilman,et al.  GAIP and RGS4 Are GTPase-Activating Proteins for the Gi Subfamily of G Protein α Subunits , 1996, Cell.

[9]  R. North,et al.  D2, D3, and D4 dopamine receptors couple to G protein-regulated potassium channels in Xenopus oocytes. , 1996, Molecular pharmacology.

[10]  K. Blumer,et al.  Inhibition of G-protein-mediated MAP kinase activation by a new mammalian gene family , 1996, Nature.

[11]  D. Clapham,et al.  The K+ channel inward rectifier subunits form a channel similar to neuronal G protein‐gated K+ channel , 1996, FEBS letters.

[12]  H. Horvitz,et al.  EGL-10 Regulates G Protein Signaling in the C. elegans Nervous System and Shares a Conserved Domain with Many Mammalian Proteins , 1996, Cell.

[13]  M. Lazdunski,et al.  Molecular Properties of Neuronal G-protein-activated Inwardly Rectifying K+ Channels (*) , 1995, The Journal of Biological Chemistry.

[14]  D. Clapham,et al.  Ion channel regulation by G proteins. , 1995, Physiological reviews.

[15]  K. Kameyama,et al.  Receptor kinase‐dependent desensitization of the muscarinic K+ current in rat atrial cells. , 1995, The Journal of physiology.

[16]  H. Dohlman,et al.  Inhibition of G-protein signaling by dominant gain-of-function mutations in Sst2p, a pheromone desensitization factor in Saccharomyces cerevisiae , 1995, Molecular and cellular biology.

[17]  D. Clapham,et al.  The G-protein-gated atrial K+ channel IKAch is a heteromultimer of two inwardly rectifying K+-channel proteins , 1995, Nature.

[18]  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.

[19]  Y. Jan,et al.  Activation of the cloned muscarinic potassium channel by G protein βγ subunits , 1994, Nature.

[20]  S. Heximer,et al.  A human gene encoding a putative basic helix-loop-helix phosphoprotein whose mRNA increases rapidly in cycloheximide-treated blood mononuclear cells. , 1994, DNA and cell biology.

[21]  Yoshihiro Kubo,et al.  Primary structure and functional expression of a rat G-protein-coupled muscarinic potassium channel , 1993, Nature.

[22]  T. Asano,et al.  Immunoassay for the βγ Subunits of GTP-Binding Proteins and Their Regional Distribution in Bovine Brain , 1988 .

[23]  G. Szabó,et al.  Mechanism of muscarinic receptor-induced K+ channel activation as revealed by hydrolysis-resistant GTP analogues , 1988, The Journal of general physiology.

[24]  M. McBurney,et al.  Retinoic acid induces embryonal carcinoma cells to differentiate into neurons and glial cells , 1982, The Journal of cell biology.