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Potassium inwardly-rectifying channel, subfamily J, member 1

ROMK, ROMK1, inwardly rectifying K+ channel, Kir1.1, KCNJ1
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. It is activated by internal ATP and probably plays an important role in potassium homeostasis. The encoded protein has a greater tendency to allow potassium to flow into a cell rather than out of a cell. Mutations in this gene have been associated with antenatal Bartter syndrome, which is characterized by salt wasting, hypokalemic alkalosis, hypercalciuria, and low blood pressure. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, KIR, ACID, HAD, Kir2.1
Papers on ROMK
ROMK1 Knockout Mice Do Not Produce Bartter's Phenotype But Exhibit Impaired K Excretion.
Wang et al., United States. In J Biol Chem, Feb 2016
We have generated a mouse deficient only in ROMK1 by selective deletion of the ROMK1-specific first exon using an ES cell Cre-LoxP strategy and examined the renal phenotypes, ion transporter expression, ROMK channel activity and localization under normal and high K intake.
Roles and Regulation of Renal K Channels.
Welling, Baltimore, United States. In Annu Rev Physiol, Jan 2016
Recently, a confluence of discoveries in areas from human genetics to physiology, cell biology, and biophysics has cast light on the special function of five different potassium channels in the distal nephron, encoded by the genes KCNJ1, KCNJ10, KCNJ16, KCNMA1, and KCNN3.
ROMK Inhibitor Actions in the Nephron Probed with Diuretics.
Denton et al., In Am J Physiol Renal Physiol, Jan 2016
ROMK is an attractive diuretic target, in part, because its inhibition is postulated to indirectly inhibit the bumetanide-sensitive Na(+)-K(+)-2Cl- co-transporter, NKCC2, and the amiloride- and benzamil-sensitive epithelial Na(+) channel, ENaC.
Insulin and IGF-1 activate Kir4.1/5.1 channels in cortical collecting duct principal cells to control basolateral membrane voltage.
Pochynyuk et al., Houston, United States. In Am J Physiol Renal Physiol, Jan 2016
Acute treatment with 10 μM amiloride (ENaC blocker), 100 nM Tertiapin-Q (TPNQ, ROMK inhibitor), and 100 μM ouabain (Na(+)-K(+) ATPase blocker) failed to produce a measurable effect on the macroscopic current.
Animal toxins and renal ion transport: Another dimension in tropical nephrology.
Sitprija et al., Bangkok, Thailand. In Nephrology (carlton), Oct 2015
Most renal tubular K channels including voltage gated K channels (Kv1), KATP , ROMK1, BK and SK are blocked by scorpion toxins.
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).
[EAST/SeSAME syndrome and functional expression of inward rectifier potassium channel Kir4.1 in the inner ear].
Zhao et al., In Lin Chuang Er Bi Yan Hou Ke Za Zhi, Jul 2015
The KCNJ10 gene which encodes an inwardly rectifying K+ channel Kir4.1 subunit plays an essential role in the inner ear and hearing.
Cleft Palate, Moderate Lung Developmental Retardation and Early Postnatal Lethality in Mice Deficient in the Kir7.1 Inwardly Rectifying K+ Channel.
Sepúlveda et al., Valdivia, Chile. In Plos One, 2014
Kir7.1 is an inwardly rectifying K+ channel of the Kir superfamily encoded by the kcnj13 gene.
Roles of Akt and SGK1 in the Regulation of Renal Tubular Transport.
Horita et al., Tokyo, Japan. In Biomed Res Int, 2014
In addition, SGK1 and Akt cooperatively regulate potassium secretion by renal outer medullary potassium channel (ROMK).
Inhibitors of the renal outer medullary potassium channel: a patent review.
Calderone et al., Pisa, Italy. In Expert Opin Ther Pat, 2014
In this panorama, inhibitors of the renal outer medullary potassium (ROMK) channels are emerging because they are predicted to give a diuretic/natriuretic activity higher than that provided by loop diuretics, without hypokaliemic and hyperkaliemic side effects.
Mitochondrial ROMK channel is a molecular component of mitoK(ATP).
O'Rourke et al., Baltimore, United States. In Circ Res, 2012
The findings support ROMK as the pore-forming subunit of the cytoprotective mitoK(ATP) channel in heart mitochondria.
Effects of insulin on Na and K transporters in the rat CCD.
Palmer et al., New York City, United States. In Am J Physiol Renal Physiol, 2012
Insulin also more than doubled ROMK (tertiapin-Q-sensitive) K(+) currents in kidney collecting ducts.
Activation of PI3-kinase stimulates endocytosis of ROMK via Akt1/SGK1-dependent phosphorylation of WNK1.
Huang et al., Dallas, United States. In J Am Soc Nephrol, 2011
PI3K-activating hormones inhibit ROMK by enhancing its endocytosis via a mechanism that involves phosphorylation of WNK1 by Akt1 and SGK1.
Tamm-Horsfall glycoprotein interacts with renal outer medullary potassium channel ROMK2 and regulates its function.
Waldegger et al., Marburg an der Lahn, Germany. In J Biol Chem, 2011
THGP modulation of ROMK function confers a new role of THGP on renal ion transport and may contribute to salt wasting observed in FJHN/MCKD-2/GCKD patients.
DNA analysis of renal electrolyte transporter genes among patients suffering from Bartter and Gitelman syndromes: summary of mutation screening.
Ryšavá et al., Praha, Czech Republic. In Folia Biol (praha), 2010
no mutation in the KCNJ1 gene, among patients suffering from bartter and Gitelman syndromes
Rare independent mutations in renal salt handling genes contribute to blood pressure variation.
Lifton et al., New Haven, United States. In Nat Genet, 2008
Members of the Framingham Heart Study were screened for variation in three genes-SLC12A3, SLC12A1 and KCNJ1 causing rare recessive diseases featuring large reductions in blood pressure.
Mouse models and the urinary concentrating mechanism in the new millennium.
Knepper et al., Århus, Denmark. In Physiol Rev, 2007
These include the major renal water channels (aquaporins), urea transporters, ion transporters and channels (NHE3, NKCC2, NCC, ENaC, ROMK, ClC-K1), G protein-coupled receptors (type 2 vasopressin receptor, prostaglandin receptors, endothelin receptors, angiotensin II receptors), and signaling molecules.
Molecular pathogenesis of pseudohypoaldosteronism type II: generation and analysis of a Wnk4(D561A/+) knockin mouse model.
Uchida et al., Tokyo, Japan. In Cell Metab, 2007
Apical localization of the ROMK potassium channel and transepithelial Cl(-) permeability in the cortical collecting ducts were not affected in the knockin mice, whereas activity of epithelial Na(+) channels (ENaC) was increased.
(Patho)physiological significance of the serum- and glucocorticoid-inducible kinase isoforms.
Vallon et al., Tübingen, Germany. In Physiol Rev, 2006
SGKs activate ion channels (e.g., ENaC, TRPV5, ROMK, Kv1.3, KCNE1/KCNQ1, GluR1, GluR6), carriers (e.g., NHE3, GLUT1, SGLT1, EAAT1-5), and the Na+-K+-ATPase.
WNK4 regulates the balance between renal NaCl reabsorption and K+ secretion.
Lifton et al., New Haven, United States. In Nat Genet, 2003
By expression in Xenopus laevis oocytes, we show that WNK4 also inhibits the renal K+ channel ROMK.
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