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
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
Muscarinic inhibition of calcium current and M current in Galpha q-deficient mice.
Opsin-G11-mediated signaling pathway for photic entrainment of the chicken pineal circadian clock.
Signaling and ligand binding by recombinant neuromedin U receptors: evidence for dual coupling to Galphaq/11 and Galphai and an irreversible ligand-receptor interaction.
D1-D2 dopamine receptor heterooligomers with unique pharmacology are coupled to rapid activation of Gq/11 in the striatum.
Integral and associated lysosomal membrane proteins.
Recombinase-mediated cassette exchange reveals the selective use of Gq/G11-dependent and -independent endothelin 1/endothelin type A receptor signaling in pharyngeal arch development.
RGS22, a novel testis-specific regulator of G-protein signaling involved in human and mouse spermiogenesis along with GNA12/13 subunits.
Large-scale proteomics and phosphoproteomics of urinary exosomes.
Proteomic analysis of human parotid gland exosomes by multidimensional protein identification technology (MudPIT).
The Gq/G11-mediated signaling pathway is critical for autocrine potentiation of insulin secretion in mice.
In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine.
Age-dependent blood pressure elevation is due to increased vascular smooth muscle tone mediated by G-protein signalling.
Structures of the M1 and M2 muscarinic acetylcholine receptor/G-protein complexes.
Type II adenylylcyclase integrates coincident signals from Gs, Gi, and Gq.
Interaction between G proteins and tyrosine kinases upon T cell receptor.CD3-mediated signaling.
Interaction of the G-protein G11alpha with receptors and phosphoinositidase C: the contribution of G-protein palmitoylation and membrane association.
The receptor:G-protein complex dissociates
Thrombin-activated PARs activate Gq
PLC-beta hydrolyses PIP2 to DAG and IP3
The high affinity receptor complex binds to G-protein
G-protein alpha subunit is inactivated
The receptor:G-protein complex releases GDP
The receptor:G-protein complex binds GTP
G-protein beta-gamma subunits rebind the alpha-GDP subunit
Liganded Gq/11-activating GPCRs act as GEFs for Gq/11
Thrombin-activated PARs binds G-protein Gq
Thrombin-activated PARs:Gq (active) dissociate
G alpha (q) binds to Trio family RhoGEFs
G alpha (q) inhibits PI3K alpha
GRK2 sequesters activated Gq
Dissociation of the P2Y purinoceptor 1:Gq complex
G alpha (q) auto-inactivates by hydrolysing GTP to GDP
Activated TP receptor binds G-proten Gq
Gq activation by TP receptor
Dissociation of the TP:Gq complex
P2Y purinoceptor 1 activates MAP kinase p38 alpha
Liganded Gq-activating GPCRs bind inactive heterotrimeric Gq
The Ligand:GPCR:Gq complex dissociates
Inactive G alpha (q) reassociates with G beta:gamma
G-protein alpha releases G-protein heterotrimer from PDCL
BTK in active Gq-BTK complex is activated
Gq-BTK complex dissociates to Active BTK and Gq
Active G alpha (q) binds RGS proteins
G alpha (q) in G (q):RGS complex is inactivated
G alpha (q):RGS dissociates to inactive G alpha (q)
Using siRNA to define functional interactions between melanopsin and multiple G Protein partners.
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Mouse cellular assays establish separate Gnaq and Gna11 melanopsin-signaling capacity; native combined knockdown supports overlapping contributions, with human involvement inferred comparatively.
"These data confirm that Gnaq and Gna11 convey the melanopsin signal in Neuro-2A cells."
Loss of gq/11 genes does not abolish melanopsin phototransduction.
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Retained responses after tested mouse single/double losses constrain essentiality; possible compensation prevents interpreting these results as absence of participation.
"Another possibility is that there is compensatory upregulation from other remaining Gq/11 family members in the tested mutant lines."