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Pathogenic Gαo Mutants Drive Dominant GPCR Coupling in GNAO1 Encephalopathies
Yonika A. Larasati
, Camille Rabesahala de Meritens
, Miriam Stoeber
,
Vladimir L. Katanaev
*
, Gonzalo P. Solis
*
*
Corresponding author for this work
QBRI - Translational Oncology Research Center
University of Geneva
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Keyphrases
G Protein-coupled Receptor
100%
GNAO1 Encephalopathy
100%
Dystonia
50%
G Protein
50%
Bimolecular Fluorescence Complementation (BiFC)
50%
Split YFP
50%
Phosphorylation
25%
Plasma Membrane
25%
Protein Complex
25%
Sequester
25%
Heterozygous mutation
25%
Underlying Disease
25%
Receptor Phosphorylation
25%
Infantile Epileptic Encephalopathy
25%
Biosensor Assay
25%
Receptor-mediated Endocytosis
25%
GNAO1
25%
Go Protein
25%
Receptor Internalization
25%
Protein Behavior
25%
Functional Disruption
25%
Immunology and Microbiology
Cell Membrane
100%
Internalization
100%
Endocytosis
100%
Protein Complex
100%
Biochemistry, Genetics and Molecular Biology
G Protein Coupled Receptor
100%
Bimolecular Fluorescence Complementation
50%
Cell Membrane
25%
Endocytosis
25%
Internalization
25%
Protein Complexes
25%
Heterotrimeric G Protein
25%
Genetic Disorder
25%
G Protein
25%