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the present results implicate GNAI3 as a critical regulator of odonto/osteogenic differentiation of stem cells from the apical papilla in tooth root development.
These results delineate a role for Galphai2 in early thymocyte development and for Galphai2/3 in multiple aspects of T cell biology.
direct binding of GATA4 to the GNAI3 promoter, both in vitro and in vivo, is reported.
Gpsm2 defines an approximately 200 nm nanodomain at the tips of stereocilia and this localization requires the presence of Galphai3, myosin 15 and whirlin.
this study shows that Galphai3-deficient neutrophils display reduced transmigration but normal arrest
GIV and its substrate Galphai3 are recruited to active integrin complexes
Data show that disrupting resistance to inhibitors of cholinesterase 8A (Ric-8A) expression in hematopoietic cells results in a loss of GTP-binding protein alpha subunits Galphai2, Galphai3, and Galphaq.
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 and Galphai3, indicating important roles for both Galphai isoforms.
The absence of Galphai2 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 and its partner Galpha-inhibiting activity polypeptide 3 (GNAI3) are involved in zVAD-, but not TNF-, induced cell death.
support for the hitherto untested model that Par3-mInsc and Galphai3 act cooperatively to polarize LGN 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, or RGS19; 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-/- 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.
Primary cilium migration depends on Gnai3 signaling control of subapical cytoskeleton.
Mice with mutations of Gnai1 or Gnai2 have neither fusions of ribs nor lumbar vertebrae, but loss of both Gnai3 and one of the other two genes increases the number and severity of rib fusions without affecting the lumbar fusions.
Wild-type and Galphai3-deficient mice do not exhibit reduced recruitment of macrophages in experimental models of thioglycollate-induced peritonitis and lipopolysaccharide-triggered lung injury.
analysis of Galphai2- and Galphai3-specific regulation of voltage-dependent L-type calcium channels in cardiomyocytes
These results identify the Oa1 transducer Galphai3 as the first downstream component in the Oa1 signaling pathway.
magnetic field-dependent nuclear magnetic resonance relaxation analyses were used to investigate the structural and dynamic properties of GDP bound Galpha on a microsecond timescale.
Results show that Galphai3 nuclear translocation causes irradiation resistance in human glioma cells through its complexation with DNA-PKcs leading to DNA repair.
GNAI3 is identified a second gene possibly responsible for X-linked ocular albinism.
These data indicate that, unlike in taste cells, TAS2Rs couple to the prevalent G proteins, Galphai1, Galphai2, and Galphai3, with no evidence for functional coupling to Galphagust.
Data show that auriculo-condylar syndrome (ACS)-associated mutations in G protein subunit alpha i3 (GNAI3) produce dominant-negative Galpha(i3) mutant proteins that couple to endothelin type A receptor (ET(A)R).
In postmortem human prefrontal cortex, adenosine A1 receptor is coupled preferentially, if not exclusively, to Galphai-3.
transcriptional upregulation of Girdin expression and Girdin-Galphai3 signaling play crucial roles in regulating epithelial apicobasal polarity through the PAR complex.
We demonstrate that the GNAI3 variant is the likely cause of auriculocondylar syndrome in the original ACS1 family.
Both SH2 and GEF domains of GIV are required for the formation of a ligand-activated ternary complex between GIV, Galphai3, and EGFR.
Low GNAI3 expression is associated with hepatocellular carcinoma.
We observed increased expression of Galphai1/3 in wounded human skin and keloid skin tissues, suggesting the possible involvement of Galphai1/3 in wound healing and keloid formation.
Data indicate that dynein- and astral microtubule-mediated transport of Galphai/LGN/nuclear mitotic apparatus (NuMA) 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 and GNAI3, should be considered as potential candidates for other ear and jaw malformations.
The mechanisms of regulation of GIRK by Galpha(i/o) using wild-type Galpha(i3) (Galpha(i3)WT) and Galpha(i3), were investigated.
These results provide mechanistic insights into how reversible modulation of Galpha(i3) activity by AGS3 and GIV maintains the delicate equilibrium between promotion and inhibition of autophagy.
Data suggest that Galphai-TNFAIP8-mediated rescue of pre-oncogenic cells enhances progression to oncogenic transformation, providing a selective target to inhibit cellular transformation.
we show that A3 adenosine receptor/Gi3 play important roles in human mast cells responses initiated on contact with activated T cells.
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