Potassium Inwardly-Rectifying Channel, Subfamily J, Member 6 Protéines (KCNJ6)

Human Potassium Inwardly-Rectifying Channel, Subfamily J, Member 6 (KCNJ6) interaction partners

1. Gi/o-coupled muscarinic receptors co-localize with GIRK channel for efficient channel activation

2. The KCNJ6 -1250A and COMT Val alleles are predisposing preterm newborns to diminished opioid-induced pain relief.

3. The major findings of the current study are 1) an additive genotypic effect of the KCNJ6 SNP on the ERO theta power phenotype during reward processing, increasing significantly across genotypes.

4. Three of the four KCNJ6 SNPs studied here were found to be significantly associated with the same theta event related oscillations in adults.

5. The findings of this study suggest that variations in KCNJ6 genes are associated with both mild and severe persistent breast pain after breast cancer surgery.

6. KCNJ6 (GIRK2) gene polymorphism rs2835859 could serve as a marker that predicts sensitivity to analgesics and pain and susceptibility to nicotine dependence.

7. In this transgenic mouse model, GIRK2 plays a major role in the genesis of infantile spasms.

8. Keppen-Lubinsky syndrome is caused by mutations in the inwardly rectifying K+ channel encoded by KCNJ6.

9. For KCNJ6, three SNPs (i.e., rs2835914, rs8129919, rs2836050) were associated with the occurrence of preoperative breast pain.

10. Eight KCNNJ6 single nucleotide polymorphisms(SNPs) are significantly associated with pain-related phenotypes.

11. Ethanol associates directly with the GIRK channel, leading to enhanced interaction with a membrane phospholipid phosphatidylinositol 4,5-bisphosphate and activation of the channel.

12. 3.5 A resolution crystal structure of the mammalian GIRK2 channel in complex with betagamma G-protein subunits, the central signalling complex that links G-protein-coupled receptor stimulation to K(+) channel activity

13. KCNJ6 (or its product GIRK2) accounts for some of the variations in frontal theta; band oscillations.

14. Conformational information encoded by ligand binding to delta-opioid receptors (DORs) is transmitted to Kir3.1/Kir3.2 channels.

15. GIRK2 is expressed in nearly every human pigmented neuron or mouse tyrosine hydroxylase-immunoreactive neuron in both the substantia nigra and ventral tegmental areas.

16. GIRK overexpression in Ts65Dn mice has functional consequences affecting balance between GABA(A) and GABA(B) inhibition of CA1 pyramidal neurons in a pathway specific manner, that may contribute to cognitive deficits in Ts65 mouse model of Down syndrome.

17. KCNJ6 is associated with alcohol dependence and may moderate the effect of early psychosocial stress on risky alcohol drinking in adolescents

18. This study is the first to identify the expression of GIRK2-4 subunits in human esophageal smooth muscle cells.

19. The KCNJ6 promoter is activated by Trichostatin A (TSA) treatment and by serum depletion according to promoter reporter assays in HEK 293 cells.

20. significant interaction between the TT genotype of rs2070995 (located in KCNJ6) and the GG genotype of rs2253206 (located in CREB1) on rumination were found

Mouse (Murine) Potassium Inwardly-Rectifying Channel, Subfamily J, Member 6 (KCNJ6) interaction partners

1. These results reveal selective small molecule binding and uncover a mechanism by which rotation of the cytoplasmic domain can modulate GIRK*phosphatidylinositide interactions.

2. The results of this study indicated that Kcnj6 triploid mice show an increase in GIRK2 protein levels compared to WT mice in the cortex and thalamus.

3. GIRK2 isoform balance within a neuron can impact the processing of afferent inhibitory input and associated behavior.

4. Locomotor activity of the mice was not changed compared to that of GIRK2(floxed) mice, when tested in the open field

5. Results indicate that the properties and inhibitory activity of dorsal raphe neurons are highly regulated by G protein-coupled inwardly rectifying K+ (GIRK) 2 subunit-containing channels, introducing GIRK channels as potential candidates for studying the pathophysiology and treatment of affective disorders.

6. Increased Kcnj6 gene dose is necessary for synaptic and cognitive dysfunction in the animal model of Down Syndrome.

7. The GABABR-coupled GIRK2 channel is necessary for the GABABR agonist-induced infantile spasms phenotype in the Ts mouse and may represent a novel therapeutic target for the treatment of infantile spasms in Down syndrome.

8. It was concluded that GIRK2, through its dual responsiveness to G protein beta-gamma and Na+, mediates a form of neuronal inhibition that is amplifiable in the setting of excess electrical activity.

9. cholesterol did not affect the unitary conductance of GIRK2, it significantly enhanced the frequency of channel openings.

10. Results indicate that GIRK channels formed by GIRK2 subunits determine depression-related behaviors as well as basal and 5-HT1A receptor-mediated dorsal raphe neuronal activity

11. This study showed that spontaneous GIRK2 mutations causing cerebellar pathology are impaired in motor functions during the neonatal period.

12. This study demonstrated that the residue Ser-196 in Kir3.2 is involved in conferring PKC-mediated inhibition to the channel.

13. In the ventral tegmental area, GABA neurons express both GIRK2 (and GIRK1) subunits.

14. Gbeta-gamma and PIP2 must be present simultaneously to activate GIRK2.

15. Ligand-operated activation of Kir3.2 appears to cause dilation of the pore at the cytoplasmic domain, and is regulated conformationally.

16. A subcellular GIRK2c/GIRK3 pathway is identified that regulates excitability of ventral tegmental area dopamine neurons.

17. The results of this study show that Girk2 gene mutation alters electric activity of LC neurons in vivo.

18. Altogether, these findings shed new light on the developmental regulation of GIRK channels in the cerebellum

19. In the dorsal horn of the developing rat, K(ir)3.1 and K(ir)3.2 were expressed at mature levels from birth.

20. GIRK2 mediates the mGluR-sensitive current in unipolar brush cells