Gene Ontology annotation through association of InterPro records with GO terms
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
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
The G-protein regulator AGS3 controls an early event during macroautophagy in human intestinal HT-29 cells.
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AGS3 stabilizes GDP-bound Gai3 in a pathway controlling macroautophagy in HT-29 cells.
"AGS3 contains GoLoco or G-protein regulatory motifs in its COOH-terminal half that stabilize the GDP-bound conformation of the alpha-subunit of the trimeric Gi3 protein. The latter is part of a signaling pathway that controls the lysosomal-autophagic catabolism in human colon cancer HT-29 cells."
Localization of Gi alpha proteins in the centrosomes and at the midbody: implication for their role in cell division.
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Gai1-3 localize to centrosomes and midbody; Gai3 overexpression prolongs mitosis.
"We show expression of G(ialpha1), G(ialpha2), and G(ialpha3) in the centrosomes and at the midbody."
Integral and associated lysosomal membrane proteins.
Structural diversity in the RGS domain and its interaction with heterotrimeric G protein alpha-subunits.
Large-scale proteomics and phosphoproteomics of urinary exosomes.
Structural determinants of G-protein alpha subunit selectivity by regulator of G-protein signaling 2 (RGS2).
Defining the membrane proteome of NK cells.
MHC class II-associated proteins in B-cell exosomes and potential functional implications for exosome biogenesis.
Toward an understanding of the protein interaction network of the human liver.
A proteome-scale map of the human interactome network.
Daple is a novel non-receptor GEF required for trimeric G protein activation in Wnt signaling.
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DAPLE activates Gai via a GBA motif downstream of Frizzled.
"Daple contains a Gα-binding and activating (GBA) motif, which activates Gαi proteins"
GIV/Girdin activates Gαi and inhibits Gαs via the same motif.
Membrane Recruitment of the Non-receptor Protein GIV/Girdin (Gα-interacting, Vesicle-associated Protein/Girdin) Is Sufficient for Activating Heterotrimeric G Protein Signaling.
Architecture of the human interactome defines protein communities and disease networks.
A biochemical and genetic discovery pipeline identifies PLCδ4b as a nonreceptor activator of heterotrimeric G-proteins.
Molecular cloning of a new human G protein. Evidence for two Gi alpha-like protein families.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
Differential coupling of m2 and m4 muscarinic receptors to inhibition of adenylyl cyclase by Gi alpha and G(o)alpha subunits.
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m2 muscarinic receptors couple to adenylyl cyclase inhibition via Gai3.
"We found that both the chick and human m2 mAChRs can couple to Gi alpha-1, Gi alpha-2, Gi alpha-3, and G(o)alpha"
Adenylate cyclase increases the GTPase activity of G alpha-olf
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
RGS10 is a selective activator of G alpha i GTPase activity.
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RGS10 binds activated Gai3 and accelerates its GTP hydrolysis (GAP activity).
"RGS10 increases potently and selectively the GTP hydrolytic activity of several members of the G alphai family, including G alphai3, G alphaz, and G alpha0."
GIV is a nonreceptor GEF for G alpha i with a unique motif that regulates Akt signaling.
A G{alpha}i-GIV molecular complex binds epidermal growth factor receptor and determines whether cells migrate or proliferate.
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Gai, GIV and EGFR assemble a signaling complex when the GIV GEF motif is intact.
"a Galpha(i)-GIV-EGFR signaling complex assembles"
Molecular architecture of the Gα(i)-bound TRPC5 ion channel.
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Cryo-EM structure of TRPC5 bound to Gai3; Gai3 sensitizes TRPC5 to PIP2.
"Electrophysiological analysis shows that Gαi3 increases the sensitivity of TRPC5 to phosphatidylinositol 4,5-bisphosphate (PIP2)"
A human homeotic transformation resulting from mutations in PLCB4 and GNAI3 causes auriculocondylar syndrome.
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A recurrent GNAI3 missense variant causes auriculocondylar syndrome.
"identified two novel (exclusive to the patient and/or family studied) missense mutations in PLCB4 and a shared mutation in GNAI3 in two unrelated probands"
Heterogeneity of mutational mechanisms and modes of inheritance in auriculocondylar syndrome.
Recombinant alpha i-3 subunit of G protein activates Gk-gated K+ channels.
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Activated recombinant ai-3 stimulated atrial K+ channel currents in excised patches (historical claim; GIRK activation is now attributed mainly to Gbetagamma).
"r alpha i-3, activated either by guanosine 5'-(3-thio)triphosphate (GTP gamma S) or AlF-4, stimulated in a concentration-dependent manner single channel K+ currents in isolated atrial membrane patches"
UniProtKB P08754 (GNAI3_HUMAN) flat file
Distinct patterns of bidirectional regulation of mammalian adenylyl cyclases.
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Purified Gi alpha 1, 2 and 3 inhibit reconstituted adenylyl cyclases, types V and VI most strongly; type II is resistant.
"Types V and VI adenylyl cyclase are most sensitive to inhibition by Gi alpha 1, Gi alpha 2, and Gi alpha 3"