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1
Deletion of the Cl-/HCO3- exchanger pendrin downregulates calcium-absorbing proteins in the kidney and causes calcium wasting.
Nephrol Dial Transplant. 2012 Apr;27(4):1368-79. doi: 10.1093/ndt/gfr505. Epub 2011 Aug 26.
3
Ablation of the Cl-/HCO3- Exchanger Pendrin Enhances Hydrochlorothiazide-Induced Diuresis.
Kidney Blood Press Res. 2017;42(3):444-455. doi: 10.1159/000479296. Epub 2017 Jul 27.
6
The role of pendrin in renal physiology.
Annu Rev Physiol. 2015;77:363-78. doi: 10.1146/annurev-physiol-021014-071854.
7
Lack of pendrin HCO3- transport elevates vestibular endolymphatic [Ca2+] by inhibition of acid-sensitive TRPV5 and TRPV6 channels.
Am J Physiol Renal Physiol. 2007 May;292(5):F1314-21. doi: 10.1152/ajprenal.00432.2006. Epub 2007 Jan 2.
9
Decreased expression of Slc26a4 (Pendrin) and Slc26a7 in the kidneys of carbonic anhydrase II-deficient mice.
Cell Physiol Biochem. 2008;21(1-3):95-108. doi: 10.1159/000113751. Epub 2008 Jan 16.

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2
OXGR1 is a candidate disease gene for human calcium oxalate nephrolithiasis.
Genet Med. 2023 Mar;25(3):100351. doi: 10.1016/j.gim.2022.11.019. Epub 2022 Dec 6.
3
Regulation of urinary calcium excretion by vasopressin.
Clin Kidney J. 2020 Sep 16;13(5):873-877. doi: 10.1093/ckj/sfaa134. eCollection 2020 Oct.
4
Importance of SLC26 Transmembrane Anion Exchangers in Sperm Post-testicular Maturation and Fertilization Potential.
Front Cell Dev Biol. 2019 Oct 18;7:230. doi: 10.3389/fcell.2019.00230. eCollection 2019.
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The non-diuretic hypotensive effects of thiazides are enhanced during volume depletion states.
PLoS One. 2017 Jul 18;12(7):e0181376. doi: 10.1371/journal.pone.0181376. eCollection 2017.
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Acid Load and Phosphorus Homeostasis in CKD.
Am J Kidney Dis. 2017 Oct;70(4):541-550. doi: 10.1053/j.ajkd.2017.04.022. Epub 2017 Jun 21.
7
Prostaglandin-E2 Mediated Increase in Calcium and Phosphate Excretion in a Mouse Model of Distal Nephron Salt Wasting.
PLoS One. 2016 Jul 21;11(7):e0159804. doi: 10.1371/journal.pone.0159804. eCollection 2016.
8
Distal convoluted tubule.
Compr Physiol. 2015 Jan;5(1):45-98. doi: 10.1002/cphy.c140002.
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Molecular mechanisms and regulation of urinary acidification.
Compr Physiol. 2014 Oct;4(4):1737-74. doi: 10.1002/cphy.c140021.
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The role of drug transporters in the kidney: lessons from tenofovir.
Front Pharmacol. 2014 Nov 11;5:248. doi: 10.3389/fphar.2014.00248. eCollection 2014.

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1
Nephrolithiasis-associated bone disease: pathogenesis and treatment options.
Kidney Int. 2011 Feb;79(4):393-403. doi: 10.1038/ki.2010.473. Epub 2010 Dec 1.
2
The renal connecting tubule: Resolved and unresolved issues in Ca(2+) transport.
Int J Biochem Cell Biol. 2011 Jan;43(1):1-4. doi: 10.1016/j.biocel.2010.10.006. Epub 2010 Oct 20.
3
Clinical practice. Calcium kidney stones.
N Engl J Med. 2010 Sep 2;363(10):954-63. doi: 10.1056/NEJMcp1001011.
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Evidence for altered renal tubule function in idiopathic calcium stone formers.
Urol Res. 2010 Aug;38(4):263-9. doi: 10.1007/s00240-010-0299-9. Epub 2010 Jul 15.
5
Calcium oxalate stone formation in the inner ear as a result of an Slc26a4 mutation.
J Biol Chem. 2010 Jul 9;285(28):21724-35. doi: 10.1074/jbc.M110.120188. Epub 2010 May 4.
7
Testosterone increases urinary calcium excretion and inhibits expression of renal calcium transport proteins.
Kidney Int. 2010 Apr;77(7):601-8. doi: 10.1038/ki.2009.522. Epub 2010 Jan 20.
8
Deletion of the chloride transporter slc26a7 causes distal renal tubular acidosis and impairs gastric acid secretion.
J Biol Chem. 2009 Oct 23;284(43):29470-9. doi: 10.1074/jbc.M109.044396. Epub 2009 Sep 1.
9
Slc26a9--anion exchanger, channel and Na+ transporter.
J Membr Biol. 2009 Apr;228(3):125-40. doi: 10.1007/s00232-009-9165-5. Epub 2009 Apr 14.
10
Deletion of the chloride transporter Slc26a9 causes loss of tubulovesicles in parietal cells and impairs acid secretion in the stomach.
Proc Natl Acad Sci U S A. 2008 Nov 18;105(46):17955-60. doi: 10.1073/pnas.0800616105. Epub 2008 Nov 12.

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