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Guanine nucleotide-binding proteins (G proteins) are involved as modulators or transducers in various transmembrane signaling pathways. Additionally we are shipping GNAI3 Proteins (10) and GNAI3 Kits (3) and many more products for this protein.
Showing 10 out of 43 products:
Human Polyclonal GNAI3 Primary Antibody for WB - ABIN516102
Demir, Donner, Kivipelto, Kuismin, Schalin-Jäntti, De Menis, Karhu: Mutation analysis of inhibitory guanine nucleotide binding protein alpha (GNAI) loci in young and familial pituitary adenomas. in PLoS ONE 2014
GIV (show CCDC88A Antibodies) and its substrate Galphai3 are recruited to active integrin complexes
Data show that disrupting resistance to inhibitors of cholinesterase 8A (Ric-8A (show RIC8A Antibodies)) expression in hematopoietic cells results in a loss of GTP-binding protein (show DRG1 Antibodies) alpha subunits Galphai2 (show GNAI2 Antibodies), Galphai3, and Galphaq (show GNAQ Antibodies).
Data show that guanine nucleotide-binding protein G(i) subunit alpha-1 and alpha-3 (Galphai1/3) can interact with CD14 antigen/Grb2-associated binding protein Gab1, which modulates macrophage polarization in vitro and in vivo.
Myocardial ischemia promptly regulated cardiac mRNA and with a slight delay protein levels of both Galphai2 (show GNAI2 Antibodies) and Galphai3, indicating important roles for both Galphai isoforms.
The absence of Galphai2 (show GNAI2 Antibodies) and Galphai3 in B cells profoundly disturbs the architecture of lymphoid organs with loss of B cell compartments in the spleen, thymus, lymph nodes, and gastrointestinal tract.
RGS19 (show RGS19 Antibodies) and its partner Galpha (show SUCLG1 Antibodies)-inhibiting activity polypeptide 3 (show CYP Antibodies) (GNAI3) are involved in zVAD-, but not TNF (show TNF Antibodies)-, induced cell death.
support for the hitherto untested model that Par3 (show F2RL2 Antibodies)-mInsc (show INSC Antibodies) and Galphai3 act cooperatively to polarize LGN (show GPSM2 Antibodies) and promote perpendicular divisions
level of basal autophagy, autophagic induction, autophagic flux, autophagic degradation and the anti-autophagic action in macrophages that lacked Galphai3, AGS3 (show GPSM1 Antibodies), or RGS19 (show RGS19 Antibodies); or had been treated with pertussis toxin, were similar to controls
A constitutively active Galphai3 protein corrects the abnormal retinal pigment epithelium phenotype of Oa1 (show GPR143 Antibodies)-/- mice.
By using mice deficient in individual Galphai/o G-protein subunits, authors demonstrate that Galphai1 and Galphai3 are the critical in vivo targets of ADP-ribosylation underlying vasoactive amine sensitization elicited by pertussis toxin exposure.
Data show that auriculo-condylar syndrome (ACS (show PLA2G15 Antibodies))-associated mutations in G protein subunit alpha i3 (GNAI3) produce dominant-negative Galpha (show SUCLG1 Antibodies)(i3) mutant proteins that couple to endothelin type A receptor (ET(A (show EDNRA Antibodies))R).
In postmortem human prefrontal cortex, adenosine A1 receptor (show ADORA1 Antibodies) is coupled preferentially, if not exclusively, to Galphai-3.
transcriptional upregulation of Girdin (show CCDC88A Antibodies) expression and Girdin (show CCDC88A Antibodies)-Galphai3 signaling play crucial roles in regulating epithelial apicobasal polarity through the PAR (show JTB Antibodies) complex.
We demonstrate that the GNAI3 variant is the likely cause of auriculocondylar syndrome in the original ACS1 family.
Both SH2 and GEF (show SLC2A4RG Antibodies) domains of GIV (show CCDC88A Antibodies) are required for the formation of a ligand-activated ternary complex between GIV (show CCDC88A Antibodies), Galphai3, and EGFR (show EGFR Antibodies).
Low GNAI3 expression is associated with hepatocellular carcinoma.
Data indicate that dynein- and astral microtubule-mediated transport of Galphai/LGN (show GPSM2 Antibodies)/nuclear mitotic apparatus (NuMA (show NUMA1 Antibodies)) complex from cell cortex to spindle poles.
The phenotypic variability of auriculocondylar syndrome suggests that mutations in this pathway, especially those affecting core signaling molecules such as PLCB4 (show PLCb4 Antibodies) and GNAI3, should be considered as potential candidates for other ear and jaw malformations.
These results identify the Oa1 (show GPR143 Antibodies) transducer Galphai3 as the first downstream component in the Oa1 (show GPR143 Antibodies) signaling pathway.
Guanine nucleotide-binding proteins (G proteins) are involved as modulators or transducers in various transmembrane signaling pathways. G proteins are composed of 3 units: alpha, beta and gamma. This gene encodes an alpha subunit and belongs to the G-alpha family. Mutation in this gene, resulting in a gly40-to-arg substitution, is associated with auriculocondylar syndrome, and shown to affect downstream targets in the G protein-coupled endothelin receptor pathway.
guanine nucleotide binding protein (G protein), alpha inhibiting activity polypeptide 3
, guanine nucleotide-binding protein G(k) subunit alpha-like
, g(i) alpha-3
, guanine nucleotide binding protein, alpha inhibiting 3
, guanine nucleotide-binding protein G(k) subunit alpha
, Gi3 protein alpha-subunit
, guanine nucleotide binding protein alpha inhibiting 3
, G protein alpha subunit
, Guanine nucleotide binding, protein, alpha inhibiting polypeptide 3
, guanine nucleotide binding protein (G protein), alpha inhibiting 3
, alpha-subunit of G-protein, type G-alpha-i-3