Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Gene Ontology annotation based on curation of intracellular localizations of expressed fusion proteins in living cells
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
A mammalian Partner of inscuteable binds NuMA and regulates mitotic spindle organization.
Structural determinants for GoLoco-induced inhibition of nucleotide release by Galpha subunits.
Activation-induced subcellular redistribution of G alpha(s) is dependent upon its unique N-terminus.
Signaling and ligand binding by recombinant neuromedin U receptors: evidence for dual coupling to Galphaq/11 and Galphai and an irreversible ligand-receptor interaction.
Mammalian Pins is a conformational switch that links NuMA to heterotrimeric G proteins.
EP(4) prostanoid receptor coupling to a pertussis toxin-sensitive inhibitory G protein.
Localization of Gi alpha proteins in the centrosomes and at the midbody: implication for their role in cell division.
Integral and associated lysosomal membrane proteins.
Structural diversity in the RGS domain and its interaction with heterotrimeric G protein alpha-subunits.
Lactate inhibits lipolysis in fat cells through activation of an orphan G-protein-coupled receptor, GPR81.
Large-scale proteomics and phosphoproteomics of urinary exosomes.
Structural evidence for a sequential release mechanism for activation of heterotrimeric G proteins.
Differentiation of human T cells alters their repertoire of G protein alpha-subunits.
Toward an understanding of the protein interaction network of the human liver.
Chromosome- and spindle-pole-derived signals generate an intrinsic code for spindle position and orientation.
Crystal structures of the scaffolding protein LGN reveal the general mechanism by which GoLoco binding motifs inhibit the release of GDP from Gαi.
Cortical dynein is critical for proper spindle positioning in human cells.
Dynamics of Gαi1 interaction with type 5 adenylate cyclase reveal the molecular basis for high sensitivity of Gi-mediated inhibition of cAMP production.
Cortical dynein and asymmetric membrane elongation coordinately position the spindle in anaphase.
A proteome-scale map of the human interactome network.
Differential contribution of Gαi/o subunits in the response to food deprivation.
Comprehensive analysis of heterotrimeric G-protein complex diversity and their interactions with GPCRs in solution.
SAPCD2 Controls Spindle Orientation and Asymmetric Divisions by Negatively Regulating the Gαi-LGN-NuMA Ternary Complex.
Presence of three distinct molecular species of Gi protein alpha subunit. Structure of rat cDNAs and human genomic DNAs.
Architecture of the human interactome defines protein communities and disease networks.
Human cDNA clones for an alpha subunit of Gi signal-transduction protein.
GTP-binding proteins in human platelet membranes serving as the specific substrate of islet-activating protein, pertussis toxin.
A reference map of the human binary protein interactome.
Structures of the human dopamine D3 receptor-G(i) complexes.
Structural insights into the human D1 and D2 dopamine receptor signaling complexes.
Structural insights into the lipid and ligand regulation of serotonin receptors.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Structural basis for recognition of anti-migraine drug lasmiditan by the serotonin receptor 5-HT(1F)-G protein complex.
Pediatric Encephalopathy: Clinical, Biochemical and Cellular Insights into the Role of Gln52 of GNAO1 and GNAI1 for the Dominant Disease.
Structure, function and pharmacology of human itch receptor complexes.
Activation and allosteric regulation of the orphan GPR88-Gi1 signaling complex.
Molecular insights into ligand recognition and activation of chemokine receptors CCR2 and CCR3.
Structural insight into apelin receptor-G protein stoichiometry.
Structural genomics of the human dopamine receptor system.
Structure-based design of non-hypertrophic apelin receptor modulator.
A gut-derived hormone regulates cholesterol metabolism.
Promiscuous G-protein activation by the calcium-sensing receptor.
Multimodal cell maps as a foundation for structural and functional genomics.
Distinct patterns of bidirectional regulation of mammalian adenylyl cyclases.
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Purified G alpha effects depend on cyclase isoform and concentration.
"Type II adenylyl cyclase appears to be
immune to inhibition by these proteins"
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High concentrations of Gi alpha activate type I and II adenylyl cyclases through the Gs alpha site.
"High concentrations of Gi alpha can interact with site 1 on types I and II adenylyl cyclase and activate the enzymes."
RGS10 is a selective activator of G alpha i GTPase activity.
G protein-dependent activation of smooth muscle eNOS via natriuretic peptide clearance receptor.
Adenylate cyclase increases the GTPase activity of G alpha-olf
Adenylate cyclase inhibitory pathway
G alpha-olf:GTP binds to Gi alpha1:GTP:adenylate cyclase complex
Dissociation of the Gi alpha:G olf complex
Adenylate cyclase increases the GTPase activity of Gi alpha
Liganded Gi-activating GPCR acts as a GEF for Gi
Activated P2Y purinoceptor 12 binds G-protein Gi
Gi activation by P2Y purinoceptor 12
Dissociation of the P2Y purinoceptor 12:Gi complex
The Ligand:GPCR:Gi complex dissociates
Liganded Gi-activating GPCRs bind inactive heterotrimeric G-protein Gi
Inactive G alpha (i) reassociates with G beta:gamma
G protein alpha (i)-SRC complex catalyzes SRC to p-Y419-SRC
G protein alpha (i)-SRC complex dissociates to G protein alpha (i) and Active SRC
G alpha (i):RGS dissociates to inactive G alpha (i)–i1/i2/i3
Active G alpha (i)–i1/i2/i3 binds RGS proteins
G alpha (i)–i1/i2/i3 in G (i):RGS complex is inactivated
G-proteins dissociate from plasma-membrane estrogen receptors
Heterotrimeric G protein (i) binds membrane-associated ESRs:ESTG
Ligand-dependent G protein dynamics underlying opioid efficacy.
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The smFRET construct is human Gαi1 carrying R90C (AHD) and E238C (Ras-like domain) labelling sites on a minimal-cysteine background, with WT-like ligand-dependent GTP turnover.
"previously published minimal cysteine background (C3S;C66A;C214S;C350S;C325A;C351I) of human Gαi1"
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Receptor-catalysed GDP-GTP exchange on Gαi1 requires large-scale opening of the α-helical domain.
"Activation of heterotrimeric G proteins by G-protein-coupled receptors (GPCRs) requires large-scale opening of the Gα α-helical domain (AHD) to expose the nucleotide-binding site and facilitate GDP-GTP exchange"
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Ligand efficacy is encoded in the rate of AHD opening (lifetime of the closed state), not in the stability of the open state.
"Mean dwell times in this high-FRET state (τhigh) depended strongly on ligand efficacy"
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AHD transitions pass through a partly open intermediate state.
"suggesting that a partially open AHD could mediate transitions between the GDP-bound and fully open conformations"
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The relation between AHD opening and efficacy also holds for NTSR1-Gi complexes.
"Parallel smFRET imaging of NTSR1–Gi ternary complexes (Methods), which couple promiscuously in vitro, yielded a correlation between agonist-induced low-FRET occupancy and GTP turnover similar to that of μOR"
UniProtKB record for human GNAI1