Disease relevance of Kcnj6

• A cDNA clone encoding an inwardly-rectifying K-channel (BIR1) was isolated from insulinoma cells [1].
• The levels of KATP-2 mRNA were reduced by 34% in islets from diabetic Zucker diabetic fatty male rats, a model of non-insulin dependent diabetes mellitus, compared to their lean nondiabetic littermates (p < 0.05), suggesting that decreased expression of KATP-2 may contribute to beta-cell dysfunction in this animal model [2].

Psychiatry related information on Kcnj6

• Alteration in expression of G-protein-activated inward rectifier K+-channel subunits GIRK1 and GIRK2 in the rat brain following electroconvulsive shock [3].

High impact information on Kcnj6

• Adenoviral recombinants containing the cDNAs for GIRK1, GIRK2, GIRK4, and the serotonin 1A receptor were constructed [4].
• As heterotetramers, they comprise the GIRK1 and the GIRK2, -3, or -4 subunits [5].
• 2. Co-transfected cells had larger Ba2+-sensitive inwardly rectifying currents and 13 mV more negative resting potentials (in 3 mM [K+]o) than non-transfected cells, or cells transfected with GIRK1 or GIRK2 alone [6].
• Current responses of GIRK2 channels activated by mu-opioid receptors were also inhibited by halothane [7].
• Acute electroconvulsive shock (a single shock) increased GIRK2 expression while causing a transient reduction of the messenger RNA abundance of GIRK1 in granule cells of the dentate gyrus [3].

Biological context of Kcnj6

• The sequence homology with KATP-1 suggests that BIR1 is a subunit of a brain and beta-cell KATP channel [1].
• We have isolated cDNA clones from a RINm5F insulinoma cell cDNA library that encode a protein, KATP-2, whose sequence shows 72% identity with the rat heart potassium channel KATP [2].
• 1. G protein-regulated inward rectifier K+ (GIRK) channels were over-expressed in dissociated rat superior cervical sympathetic (SCG) neurones by co-transfecting green fluorescent protein (GFP)-, GIRK1- and GIRK2-expressing plasmids using the biolistic technique [6].
• In the present study we have investigated the effect of electroconvulsive shock on gene expression of the G-protein-activated inward rectifier potassium channel subunits G-protein-coupled inward rectifier K+-channel (GIRK1) and GIRK2 in the rat brain using in situ hybridization and immunocytochemistry [3].

Anatomical context of Kcnj6

• Cloning of rat KATP-2 channel and decreased expression in pancreatic islets of male Zucker diabetic fatty rats [2].
• RNA blotting showed that KATP-2 mRNA was present at high levels in brain and undetectable in heart, spleen, lung, liver, skeletal muscle, kidney and testis [2].
• Chronic electroconvulsive shock (five shocks over 10 days) caused a larger increase in GIRK2 messenger RNA abundance, which was accompanied by an increase in GIRK2 immunoreactivity in the molecular layer of the dentate gyrus [3].
• No significant alterations in GIRK1 and GIRK2 messenger RNA abundance were detected in the other brain regions studied, including the CA1 and CA3 subfields of the hippocampus, the frontal-parietal cortex and piriform cortex [3].
• The expression of G-protein-gated inwardly rectifying K+ channels GIRK1 and GIRK2 mRNAs in the supraoptic nucleus of the rat and possible role involved [8].

Associations of Kcnj6 with chemical compounds

• 3. Carbachol (CCh, 1-30 microM) increased the inwardly rectifying current in 70 % of GIRK1+ GIRK2-transfected cells by 261 +/- 53 % (n = 6, CCh 30 microM) at -120 mV, but had no effect in non-transfected cells or in cells transfected with GIRK1 or GIRK2 alone [6].
• In Xenopus oocytes coinjected with poly(A)+ RNA derived from the rat cerebellum and cRNAs for the cloned G protein-gated inwardly rectifying K+ channel (GIRK), GIRK1 and GIRK2, the GABA-B agonist baclofen elicited inwardly rectifying K+ currents [9].

Analytical, diagnostic and therapeutic context of Kcnj6

• A quantitative RT-PCR assay indicated that there were 1.85 +/- 0.32 x 10(5) molecules of KATP-2 mRNA per microgram of total RNA in pancreatic islets from nondiabetic rats [2].
• The expression of G-protein-gated inwardly rectifying K channels subunits GIRK1 and GIRK2 mRNAs in the supraoptic nucleus (SON) was investigated in the rat by in situ hybridization with non-radioactive dig-labeled cRNA probes [8].

References