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Potassium inwardly-rectifying channel, subfamily J, member 16

Kir5.1, KCNJ16
inward rectifying potassium channel; may be involved in renal pH regulation [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Kir4.1, Kir2.1, KIR, SET, HAD
Papers on Kir5.1
Variability in a three-generation family with pierre robin sequence, acampomelic campomelic dysplasia, and intellectual disability due to a novel ∼1 Mb deletion upstream of SOX9, and including KCNJ2 and KCNJ16.
Laino et al., Roma, Italy. In Birth Defects Res A Clin Mol Teratol, Jan 2016
METHODS: We report a three-generation pedigree with a novel ∼1 Mb deletion upstream of SOX9 and including KCNJ2 and KCNJ16, and ascertained for dominant transmission of PRS.
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.
Insight in genome-wide association of metabolite quantitative traits by exome sequence analyses.
van Dijk et al., Leiden, Netherlands. In Plos Genet, 2015
In addition, we found three novel, suggestively significant loci: TNP1 with pyruvate (P-value  = 1.26×10-8), KCNJ16 with 3-hydroxybutyrate (P-value  = 1.65×10-8) and 2p12 locus with valine (P-value  = 3.49×10-8).
KCNJ10 determines the expression of the apical Na-Cl cotransporter (NCC) in the early distal convoluted tubule (DCT1).
Wang et al., Valhalla, United States. In Proc Natl Acad Sci U S A, 2014
Immunostaining demonstrated Kcnj10 and Kcnj16 were expressed in the basolateral membrane of DCT, and patch-clamp studies detected a 40-pS K channel in the basolateral membrane of the DCT1 of p8/p10 wild-type Kcnj10(+/+) mice (WT).
[Predication analysis of microarray data to determine altered gene profiles in liver carcinoma related to HBV-related cirrhosis].
Xu et al., Jinan, China. In Zhonghua Gan Zang Bing Za Zhi, 2014
FOXP1, SPINK1 and KCNJ16 were verified by real-time PCR as differently expressed in the two subgroups (P value =0.011, 0.002 and 0.004, respectively).
Disease-targeted sequencing of ion channel genes identifies de novo mutations in patients with non-familial Brugada syndrome.
Lin et al., Taipei, Taiwan. In Sci Rep, 2013
Five de novo mutations were identified in four genes (SCNN1A, KCNJ16, KCNB2, and KCNT1) in three BrS patients (20%).
KCNJ10 mutations display differential sensitivity to heteromerisation with KCNJ16.
Zdebik et al., London, United Kingdom. In Nephron Physiol, 2012
However, co-expression with KCNJ16 abolished function in these heteromeric channels almost completely.
Inhibition of miR-205 impairs the wound-healing process in human corneal epithelial cells by targeting KIR4.1 (KCNJ10).
Zhang et al., Valhalla, United States. In Invest Ophthalmol Vis Sci, 2012
Moreover, overexpression miR-205 antagomer enhanced the protein expression of KCNJ10 but not KCNJ16.
An autosomal recessive leucoencephalopathy with ischemic stroke, dysmorphic syndrome and retinitis pigmentosa maps to chromosome 17q24.2-25.3.
Yahyaoui et al., Rabat, Morocco. In Bmc Med Genet, 2011
Sequencing of seven candidate genes in this locus, ATP5H, FDXR, SLC25A19, MCT8, CYGB, KCNJ16 and GRIN2C, identified three missense mutations in the FDXR gene which were also found in a homozygous state in three healthy controls, suggesting that these variants are not disease-causing mutations in the family.
Renal phenotype in mice lacking the Kir5.1 (Kcnj16) K+ channel subunit contrasts with that observed in SeSAME/EAST syndrome.
Tucker et al., Paris, France. In Proc Natl Acad Sci U S A, 2011
These results highlight the important role that Kir5.1 plays as a pH-sensitive regulator of salt transport in the DCT, and the implication of these results for the correct genetic diagnosis of renal tubulopathies is discussed.
Respiratory responses to hypercapnia and hypoxia in mice with genetic ablation of Kir5.1 (Kcnj16).
Gourine et al., London, United Kingdom. In Exp Physiol, 2011
Heteromeric Kir4.1-Kir5.1 channels are highly pH sensitive within the physiological range of pH changes and are strongly expressed by the peripheral chemosensors as well as in the brainstem pH-sensitive areas which mediate respiratory responses to changes in blood and brain levels of P(CO(2))/[H(+)].
Genetic inactivation of Kcnj16 identifies Kir5.1 as an important determinant of neuronal PCO2/pH sensitivity.
Tucker et al., Perugia, Italy. In J Biol Chem, 2011
Kir5.1 may be involved in the response to hypercapnic acidosis
Astrocytes in the retrotrapezoid nucleus sense H+ by inhibition of a Kir4.1-Kir5.1-like current and may contribute to chemoreception by a purinergic mechanism.
Mulkey et al., United States. In J Neurophysiol, 2010
Heteromeric Kir4.1-Kir5.1 channels confer pH sensitivity to retrotrapezoid nucleus astrocytes.
KCNJ10 gene mutations causing EAST syndrome (epilepsy, ataxia, sensorineural deafness, and tubulopathy) disrupt channel function.
Warth et al., Regensburg, Germany. In Proc Natl Acad Sci U S A, 2010
We investigated the localization of KCNJ10 and the homologous KCNJ16 in kidney and the functional consequences of KCNJ10 mutations found in our patients with EAST syndrome.
Parathyroid carcinoma: current understanding and new insights into gene expression and intraoperative parathyroid hormone kinetics.
Olson et al., Durham, United States. In Oncologist, 2009
Specifically, using microarray transcriptome analysis of an unequivocal case of parathyroid carcinoma and a biopsy from the same patient's normal parathyroid gland, we identify APP, CDH1, KCNJ16, and UCHL1 as differentially expressed genes in parathyroid carcinoma.
Kir4.1/Kir5.1 channel forms the major K+ channel in the basolateral membrane of mouse renal collecting duct principal cells.
Paulais et al., Paris, France. In Am J Physiol Renal Physiol, 2008
the Kir4.1/Kir5.1 channel is a major component of the K(+) conductance in the basolateral membrane of mouse cortical collecting duct principal cells
Protein kinase C dependent inhibition of the heteromeric Kir4.1-Kir5.1 channel.
Jiang et al., Atlanta, United States. In Biochim Biophys Acta, 2007
these results suggest that the Kir4.1-Kir5.1 but not the homomeric Kir4.1 channel is strongly inhibited by PKC activation.
Genetic and functional linkage of Kir5.1 and Kir2.1 channel subunits.
Karschin et al., Marburg an der Lahn, Germany. In Febs Lett, 2001
We have identified several cDNAs for the human Kir5.1 subunit of inwardly rectifying K(+) channels.
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