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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Potassium inwardly-rectifying channel, subfamily J, member 8

Kir6.1, KCNJ8
an ATP-sensitive K+ channel; involved in membrane excitability [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Kir6.2, CagA, CAN, POLYMERASE, V1a
Papers on Kir6.1
Phenylephrine preconditioning in embryonic heart H9c2 cells is mediated by up-regulation of SUR2B/Kir6.2: A first evidence for functional role of SUR2B in sarcolemmal KATP channels and cardioprotection.
Jovanović et al., Belgrade, Serbia. In Int J Biochem Cell Biol, Jan 2016
Structurally, these channels are composed of pore-forming inward rectifier, Kir6.1 or Kir6.2, and a regulatory, ATP-binding subunit, SUR1, SUR2A or SUR2B.
Sensitivity of KATP channels to cellular metabolic disorders and the underlying structural basis.
Wang et al., Beijing, China. In Acta Pharmacol Sin, Jan 2016
SUR2B/Kir6.2, SUR1/Kir6.1,
Diagnostic marker signature for esophageal cancer from transcriptome analysis.
Bollschweiler et al., Köln, Germany. In Tumour Biol, Jan 2016
The markers significantly overexpressed already in earlier tumor stages (pT1-2) of both histological subtypes (n = 19) have been clustered in a "diagnostic signature": PLA2G7, PRAME, MMP1, MMP3, MMP12, LIlRB2, TREM2, CHST2, IGFBP2, IGFBP7, KCNJ8, EMILIN2, CTHRC1, EMR2, WDR72, LPCAT1, COL4A2, CCL4, and SNX10.
Topical sulfonylurea as a novel therapy for hypertrichosis secondary to diazoxide, and potentially for other conditions with excess hair growth.
Newfield, San Diego, United States. In Med Hypotheses, Dec 2015
This approach can also be applied to rare cases of Cantú syndrome, caused by mutations in ABCC9 (coding for SUR2) or in KCNJ8 (coding for Kir6.1) that is characterized by congenital hypertrichosis.
Effect of electronic stimulation at Neiguan (PC 6) acupoint on gene expression of adenosine triphosphate-sensitive potassium channel and protein kinases in rats with myocardial ischemia.
Chen et al., In J Tradit Chin Med, Oct 2015
OBJECTIVE: To investigate the effects of electronic stimulation at acupoints Neiguan (PC 6) and Lieque (LU 7) on the gene expression of the adenosine triphosphate (ATP)-Sensitive potassium channel (KATP: Kir6.1, Kir6.2, SUR2A, and SUR2B) and protein kinases (PKA, PKG, and PKCβ2) in myocardial cells of rats with myocardial ischemia (MI) induced by isoproterenol (ISO).
The Classically Cardioprotective Agent Diazoxide Elicits Arrhythmias in Type 2 Diabetes Mellitus.
Akar et al., New York City, United States. In J Am Coll Cardiol, Oct 2015
DZX-mediated proarrhythmia in T2DM was not related to changes in the messenger ribonucleic acid expression of Kir6.1, Kir6.2, SUR1A, SUR1B, SUR2A, SUR2B, or ROMK (renal outer medullary potassium channel).
ATP-sensitive potassium channels: uncovering novel targets for treating depression.
Hu et al., Nanjing, China. In Brain Struct Funct, Sep 2015
First, we showed that chronic mild stress (CMS) significantly increased the expression of hippocampal Kir6.2 and Kir6.1 subunits of K-ATP channels.
Cantú Syndrome and Related Disorders
Singh et al., Seattle, United States. In Unknown Journal, 2014
DIAGNOSIS/TESTING: The diagnosis is established based on clinical findings and confirmed by detection of a heterozygous pathogenic variant in ABCC9 or KCNJ8.
Role of ATP-sensitive K+ channels in cardiac arrhythmias.
Nakaya, Chiba, Japan. In J Cardiovasc Pharmacol Ther, 2014
Recently, it has been proposed that the gain-of-function mutation of cardiac Kir6.1 channel can be a pathogenic substrate for J wave syndromes, a cause of idiopathic ventricular fibrillation as early repolarization syndrome or Brugada syndrome, whereas loss of function of the channel mutations can underlie sudden infant death syndrome.
Focus on Kir7.1: physiology and channelopathy.
Pattnaik et al., India. In Channels (austin), 2013
Kir4.2, and Kir6.1, albeit at levels at least 50-fold lower than Kir7.1.
KATP channels and cardiovascular disease: suddenly a syndrome.
Grange et al., Saint Louis, United States. In Circ Res, 2013
Reconstitution of KATP channel activity by coexpression of members of the pore-forming inward rectifier gene family (Kir6.1,
Blockade of ATP-sensitive potassium channels prevents the attenuation of the exercise pressor reflex by tempol in rats with ligated femoral arteries.
Kaufman et al., United States. In Am J Physiol Heart Circ Physiol, 2012
Tempol attenuates the exercise pressor reflex in rats with ligated femoral arteries via effects on K(ATP) channels.
Association of muscarinic M₃ receptors and Kir6.1 with caveolae in human detrusor muscle.
Swärd et al., Lund, Sweden. In Eur J Pharmacol, 2012
Data suggest that Kir6.1 and M3 muscarinic receptor colocalize to detrusor caveolae; studies include tissue from both male and female subjects.
The role of K ATP channels on ischemia-reperfusion injury in the rat testis.
Satoh et al., Yonago, Japan. In Life Sci, 2012
Ischemia-reperfusion injury in the rat testis significantly increased the expressions of Kir6.1 protein and mRNA as well as Kir6.2 mRNA.
Molecular genetic and functional association of Brugada and early repolarization syndromes with S422L missense mutation in KCNJ8.
Antzelevitch et al., Utica, United States. In Heart Rhythm, 2012
The researchers report evidence that the KCNJ8 gene increases susceptiblity to the brugada syndrome and early repolarization syndrome.
K(ATP) channel openers in the trigeminovascular system.
Jansen-Olesen et al., Glostrup, Denmark. In Cephalalgia, 2012
K(ATP) channel subunits Kir6.1, Kir6.2, SUR1 and SUR2B were identified in the trigeminal ganglia and trigeminal nucleus caudalis.
"Benign" early repolarization versus malignant early abnormalities: clinical-electrocardiographic distinction and genetic basis.
Baranchuk et al., Santo André, Brazil. In Cardiol J, 2011
The inherited-familial forms are not frequent in IVF; however mutations were identified in the genes KCNJ8, DPP6, SCN5A, SCN3B, CACNA1C, CACNB2, and CACNA2D1.
Muscle KATP channels: recent insights to energy sensing and myoprotection.
Nichols et al., Saint Louis, United States. In Physiol Rev, 2010
Generated as complexes of Kir6.1 or Kir6.2 pore-forming subunits with regulatory sulfonylurea receptor subunits, SUR1 or SUR2, the differential assembly of K(ATP) channels in different tissues gives rise to tissue-specific physiological and pharmacological regulation, and hence to the tissue-specific pharmacological control of contractility.
ATP-sensitive potassium channels mediate survival during infection in mammals and insects.
Beutler et al., Los Angeles, United States. In Nat Genet, 2007
Study identified a profound susceptibility to infection phenotype due to a null allele of Kcnj8, encoding Kir6.1, a protein that combines with SUR2 to form an ATP-sensitive potassium channel (K(ATP)) expressed in coronary artery.
Mouse model of Prinzmetal angina by disruption of the inward rectifier Kir6.1.
Seino et al., Chiba, Japan. In Nat Med, 2002
gene disruption causes prinzmetal angina in knockout mice
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