Browse our GNAO1 Proteins (GNAO1)

Human Guanine Nucleotide Binding Protein (G Protein), alpha Activating Activity Polypeptide O (GNAO1) interaction partners

1. first report of siblings of opposite sex harboring the same GNAO1 mutation but showing differences in phenotype with pronounced dystonia in the boy and epilepsy in his sister.

2. GNAO1 transcription was inhibited by promoter hypermethylation, contributing to its low expression. It was further revealed that the silencing effect was regulated by methyltransferase 1 (DNMT1), and was further enhanced by transforming growth factor beta (TGF-beta).

3. Taken together, the data presented here suggest that TLR2 activation in human mast cells promotes the release of inflammatory mediators via distinct signaling pathways that partially depend on the action of Go proteins.

4. Study identified distinct biochemical mechanisms of pathogenic human GNAO1 mutations that may improve the understanding of the heterogeneous clinical spectrum of GNAO1-associated epilepsy and movement disorders. Furthermore, these results also carry significant implications for personalized therapeutics in GNAO1 encephalopathies.

5. The neurological phenotypes associated with GNAO1 mutations appear to lie on a spectrum, and it is possible that the c.607G>A (p.Gly203Arg) variant characterizes a phenotype with both severe epilepsy and chorea.

6. authors report 2 cases of brothers with a severe movement disorder and hypotonia without epilepsy who have been confirmed by whole exome sequencing to have a novel mutation in GNAO1

7. Phenotypic spectrum of novel GNAO1 variants in four unrelated female patients included epileptic encephalopathy and involuntary movements with severe developmental delay.

8. GNAO1 is a disease-causing gene for the autosomal dominant form of early infantile epileptic encephalopathy. The novel pathogenic variant identified in should contribute to our understanding of the expanding spectrum of infantile-onset epilepsy.

9. Endothelial cells in capillary malformations are enriched for GNAQ mutations and are likely responsible for the pathophysiology underlying capillary malformation.

10. Galphao-R243H has a mild decrease in nucleotide affinity that causes rapid nucleotide turnover and subsequent hyperactivity in cancer

11. Genetic variants of BCL2, GNAO1, and CHD2 are associated with non-obstructive azoospermia risk.

12. the present study is the first to demonstrate that GNAO1 is overexpressed in GC and that its overexpression correlates with poor prognosis, as it promotes gastric cancer cell viability.

13. Down-regulation of GNAO1 increases cell proliferation, while suppressing the senescence of hepatocellular carcinoma cells.

14. These data suggest that aberrant Galphao signaling can cause multiple neurodevelopmental phenotypes, including epileptic encephalopathy and involuntary movements.

15. Data show that HEK293T cells transfected with estrogen receptor alpha (ERalpha)+/-Galpha(o) revealed that Galpha(o) stimulated phosphorylation of ERK MAP kinases ERK 1/2 and subsequently increased the phosphorylation of ERalpha on serine 118.

16. Data reveal a change in the repertoire of Galpha(i/o) subunits during T cell differentiation and suggest functional equivalence among Galpha(i/o) subunits irrespective of their relative abundance.

17. CKbeta8- and CKbeta8-1-induced activation of ERK1/2 is mediated by the G(i)/G(o) protein, PLC, and PKCdelta.

18. a novel role in the signal transduction of thrombin receptors in HMECs (human microvascular endothelial cells) that regulates calcium signaling and cytoskeletal rearrangements

19. study suggests that one of the functions of Goalpha in the brain is to mediate extracellular signal-regulated kinase activation by G protein-coupled receptors

20. Activated Goalpha interacted directly with PLZF, and enhanced its function as a transcriptional and cell growth suppressor.

Mouse (Murine) Guanine Nucleotide Binding Protein (G Protein), alpha Activating Activity Polypeptide O (GNAO1) interaction partners

1. Galphao +/- mice developed tolerance faster and displayed more severe naltrexone-precipitated withdrawal in some behaviors than did wild-type

2. Go signaling is essential for the structural and functional integrity of the main olfactory epithelium and for specification of olfactory bulb interneurons.

3. Data obtained support the hypothesis that GalphaO-mediated signaling within the presympathetic circuits of the rostral ventral lateral medulla contributes to the autonomic control of the heart.

4. stimulation of GPR17 by the small molecule agonist MDL29,951 (2-carboxy-4,6-dichloro-1H-indole-3-propionic acid) decreases myelin basic protein expression levels mainly by triggering the Galphai/o signaling pathway.

5. Necdin is a candidate downstream effector for Galphao.

6. This heterozygous Gnao1 +/G184S mutation produces early neonatal and adult lethality accompanied by epileptiform discharges.

7. These results highlight that sensory neurons of the Galphao-expressing vomeronasal subsystem, together with the receptors they express and the molecular cues they detect, control a wide range of fundamental mating and reproductive behaviors in female mice.

8. The Goalpha expressing vomeronasal receptor cells led to all areas of the accessory olfactory bulb (AOB).

9. Data indicate that rectifying potassium channel Kir2.4 interacts with G-protein subunit Galphao.

10. Data show that Galphao is an essential requirement for the display of male-male territorial aggression as well as maternal aggression.

11. Data suggest that the novel R234H mutation imparts oncogenic properties to Galphao by accelerating nucleotide exchange and rendering it constitutively active.

12. The 2.9 A crystal structure of the enigmatic, neuronal G protein Galpha(o) in the GTP hydrolytic transition state, complexed with RGS16.

13. Go alpha subunit mainly appears to be bound to the cell membrane and concentrated in the thin finger-like dendrites of rod bipolar cells, as well as in green fluorescent protein-positive cone bipolar cells.

14. Binding of activated Galphao to GRIN1 induces activation of Cdc42, which leads to morphological changes in neuronal cells.

15. our findings establish an essential role for G(o) in the antiadrenergic effect of muscarinic agent on hyperpolarization current

16. G alpha o mediates WNT-JNK signaling through dishevelled 1 and 3, RhoA family members, and MEKK 1 and 4 in mammalian cells

17. Go2alpha optimizes vesicular filling which is instrumental for normal dopamine functioning and for the development of drug-induced behavioral sensitization.

18. Data show that Galphao colocalized with GRIN1 at neuronal dendrites and axons, and Galphao-GRIN1 pathway could mediate roles in neuronal migration and differentiation at embryonic stages.

19. Report role of Galpha0 in the control of in vivo heart rate dynamics.

20. Regulator of G protein signaling protein suppression of Galphao protein-mediated alpha2A adrenergic receptor inhibition of mouse hippocampal CA3 epileptiform activity.

Cow (Bovine) Guanine Nucleotide Binding Protein (G Protein), alpha Activating Activity Polypeptide O (GNAO1) interaction partners

1. These results indicated the interaction of GAP-43 and Galpha(o) could accelerate conversion of depalmitoylated Galpha(o) but not palmitoylated Galpha(o) from oligomers to monomers, so as to increase the GTPgammaS binding activity of Galpha(o).

Caenorhabditis elegans (C. elegans) Guanine Nucleotide Binding Protein (G Protein), alpha Activating Activity Polypeptide O (GNAO1) interaction partners

1. Exogenous arachidonoyl ethanolamide inhibits axon regeneration via the Goalpha subunit GOA-1, which antagonizes the Gqalpha subunit EGL-30.

2. Following food deprivation G protein alpha(o) is activated via RIC-8 activation.

3. findings show that the GoLoco-containing proteins GPR-1 and GPR-2, as well as the Galpha subunits GOA-1 and GPA-16, were essential for generation of proper pulling forces in asymmetric spindle positioning

4. Data show that the asymmetry of GPR-1/2 (which act with GOA-1 and GPA-16) localization depends on PAR-3 and its downstream intermediate LET-99, as well as on the MES-1/SRC-1 signaling pathway.

5. Our results suggest that EGL-47 regulates egg laying by activating Galpha(o) in the hermaphrodite-specific motor neurons to inhibit their activity.

6. down-regulation of EGL-30-DAG signaling by GOA-1 underlies olfactory adaptation and plasticity of chemotaxis

7. The stravation response is fully dependent on the subsequent activation of the G alpha(q) ortholog EGL-30.

8. These results suggest that Galpha signaling and LET-99 control centration by regulating polarized actomyosin contraction.

9. Serotonin signaling is regulated by modulating serotonin biosynthesis and Galphao and Galphaq act in the same neurons to have opposing effects on behavior, in part, by antagonistically regulating transcription of specific genes.

10. Goa-1 Goalpha and let-60 Ras act in parallel to gpc-1 in olfactory pathways.