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Journal Abstract Search

280 related items for PubMed ID: 21633011

  • 1. Renal phenotype in mice lacking the Kir5.1 (Kcnj16) K+ channel subunit contrasts with that observed in SeSAME/EAST syndrome.
    Paulais M, Bloch-Faure M, Picard N, Jacques T, Ramakrishnan SK, Keck M, Sohet F, Eladari D, Houillier P, Lourdel S, Teulon J, Tucker SJ.
    Proc Natl Acad Sci U S A; 2011 Jun 21; 108(25):10361-6. PubMed ID: 21633011
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  • 2. Role of inwardly rectifying K+ channel 5.1 (Kir5.1) in the regulation of renal membrane transport.
    Lin DH, Duan XP, Zheng JY, Wang WH.
    Curr Opin Nephrol Hypertens; 2022 Sep 01; 31(5):479-485. PubMed ID: 35894283
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  • 3. Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel.
    Wang MX, Cuevas CA, Su XT, Wu P, Gao ZX, Lin DH, McCormick JA, Yang CL, Wang WH, Ellison DH.
    Kidney Int; 2018 Apr 01; 93(4):893-902. PubMed ID: 29310825
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  • 4. Inwardly rectifying K+ channels 4.1 and 5.1 (Kir4.1/Kir5.1) in the renal distal nephron.
    Wang WH, Lin DH.
    Am J Physiol Cell Physiol; 2022 Aug 01; 323(2):C277-C288. PubMed ID: 35759440
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  • 5. [The function and regulation of basolateral Kir4.1 and Kir4.1/Kir5.1 in renal tubules].
    Xiao Y, Meng XX, Zhang H, Guo XW, Gu RM.
    Sheng Li Xue Bao; 2018 Dec 25; 70(6):600-606. PubMed ID: 30560268
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  • 6. Deletion of renal Nedd4-2 abolishes the effect of high K+ intake on Kir4.1/Kir5.1 and NCC activity in the distal convoluted tubule.
    Xiao Y, Duan XP, Zhang DD, Wang WH, Lin DH.
    Am J Physiol Renal Physiol; 2021 Jul 01; 321(1):F1-F11. PubMed ID: 34029145
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  • 7. Kir4.1/Kir5.1 Activity Is Essential for Dietary Sodium Intake-Induced Modulation of Na-Cl Cotransporter.
    Wu P, Gao ZX, Su XT, Wang MX, Wang WH, Lin DH.
    J Am Soc Nephrol; 2019 Feb 01; 30(2):216-227. PubMed ID: 30559144
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  • 8. Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4.1, ENaC, and NCC and causes hypokalemia during high HS.
    Zhang DD, Duan XP, Xiao Y, Wu P, Gao ZX, Wang WH, Lin DH.
    Am J Physiol Renal Physiol; 2021 May 01; 320(5):F883-F896. PubMed ID: 33818128
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  • 10. Deletion of Kir5.1 abolishes the effect of high Na+ intake on Kir4.1 and Na+-Cl- cotransporter.
    Duan XP, Wu P, Zhang DD, Gao ZX, Xiao Y, Ray EC, Wang WH, Lin DH.
    Am J Physiol Renal Physiol; 2021 Jun 01; 320(6):F1045-F1058. PubMed ID: 33900854
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  • 11. EAST/SeSAME Syndrome and Beyond: The Spectrum of Kir4.1- and Kir5.1-Associated Channelopathies.
    Lo J, Forst AL, Warth R, Zdebik AA.
    Front Physiol; 2022 Jun 01; 13():852674. PubMed ID: 35370765
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  • 15. Renal Tubule Nedd4-2 Deficiency Stimulates Kir4.1/Kir5.1 and Thiazide-Sensitive NaCl Cotransporter in Distal Convoluted Tubule.
    Wu P, Su XT, Gao ZX, Zhang DD, Duan XP, Xiao Y, Staub O, Wang WH, Lin DH.
    J Am Soc Nephrol; 2020 Jun 01; 31(6):1226-1242. PubMed ID: 32295826
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  • 16. Biallelic loss-of-function variants in KCNJ16 presenting with hypokalemic metabolic acidosis.
    Webb BD, Hotchkiss H, Prasun P, Gelb BD, Satlin L.
    Eur J Hum Genet; 2021 Oct 01; 29(10):1566-1569. PubMed ID: 33840812
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  • 20. Role of Angiotensin II Type 1a Receptor (AT1aR) of Renal Tubules in Regulating Inwardly Rectifying Potassium Channels 4.2 (Kir4.2), Kir4.1, and Epithelial Na+ Channel (ENaC).
    Duan XP, Xiao Y, Su XT, Zheng JY, Gurley S, Emathinger J, Yang CL, McCormick J, Ellison DH, Lin DH, Wang WH.
    Hypertension; 2024 Jan 01; 81(1):126-137. PubMed ID: 37909221
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