When proton pumps go sour: Urinary acidification and kidney stones

scientific article published on 01 May 2008

When proton pumps go sour: Urinary acidification and kidney stones is …
instance of (P31):
scholarly articleQ13442814

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P6179Dimensions Publication ID1035808071
P356DOI10.1038/KI.2008.137
P698PubMed publication ID18449176

P2093author name stringC A Wagner
P2860cites workRenal vacuolar H+-ATPaseQ34350645
Vacuolar H+ -ATPase B1 subunit mutations that cause inherited distal renal tubular acidosis affect proton pump assembly and trafficking in inner medullary collecting duct cells.Q40268734
Regions of human kidney anion exchanger 1 (kAE1) required for basolateral targeting of kAE1 in polarised kidney cells: mis-targeting explains dominant renal tubular acidosis (dRTA).Q40583048
Targeted disruption of the gene encoding the proteolipid subunit of mouse vacuolar H(+)-ATPase leads to early embryonic lethalityQ40918949
The vacuolar-ATPase B1 subunit in distal tubular acidosis: novel mutations and mechanisms for dysfunction.Q52585950
Angiotensin II stimulates vacuolar H+ -ATPase activity in renal acid-secretory intercalated cells from the outer medullary collecting duct.Q53547517
Immunohistochemical comparison of a case of inherited distal renal tubular acidosis (with a unique AE1 mutation) with an acquired case secondary to autoimmune diseaseQ79499827
Effects of human a3 and a4 mutations that result in osteopetrosis and distal renal tubular acidosis on yeast V-ATPase expression and activityQ79904229
Differential localization of vacuolar H+-ATPases containing a1, a2, a3, or a4 (ATP6V0A1-4) subunit isoforms along the nephronQ80536223
Renal acidification defects in patients with recurrent calcium nephrolithiasisQ93651154
Mutations in the gene encoding B1 subunit of H+-ATPase cause renal tubular acidosis with sensorineural deafnessQ22008703
Mutations in ATP6N1B, encoding a new kidney vacuolar proton pump 116-kD subunit, cause recessive distal renal tubular acidosis with preserved hearingQ24290187
Non-polarized targeting of AE1 causes autosomal dominant distal renal tubular acidosisQ24293024
Localization and regulation of the ATP6V0A4 (a4) vacuolar H+-ATPase subunit defective in an inherited form of distal renal tubular acidosisQ24300618
V-ATPase interacts with ARNO and Arf6 in early endosomes and regulates the protein degradative pathwayQ24301314
Familial distal renal tubular acidosis is associated with mutations in the red cell anion exchanger (Band 3, AE1) geneQ24561520
Mutations in the chloride-bicarbonate exchanger gene AE1 cause autosomal dominant but not autosomal recessive distal renal tubular acidosisQ24647772
Defects in TCIRG1 subunit of the vacuolar proton pump are responsible for a subset of human autosomal recessive osteopetrosisQ28140437
Mutations in the a3 subunit of the vacuolar H(+)-ATPase cause infantile malignant osteopetrosisQ28143618
The vacuolar (H+)-ATPases--nature's most versatile proton pumpsQ28218190
The B1-subunit of the H(+) ATPase is required for maximal urinary acidificationQ28505674
Compensatory membrane expression of the V-ATPase B2 subunit isoform in renal medullary intercalated cells of B1-deficient miceQ28588238
P433issue10
P407language of work or nameEnglishQ1860
P304page(s)1103-1105
P577publication date2008-05-01
P1433published inKidney InternationalQ6404823
P1476titleWhen proton pumps go sour: Urinary acidification and kidney stones
P478volume73

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cites work (P2860)
Q47149285F-actin reorganization by V-ATPase inhibition in prostate cancer.
Q41989687Klotho prevents renal calcium loss.
Q42430420Proteomic changes in response to crystal formation in Drosophila Malpighian tubules
Q37158489Regulation of luminal acidification by the V-ATPase

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