UNIPROT:P20020 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The kidney regulates body fluid, ion and acid/base homeostasis through the interaction of a host of channels, transporters and pumps within specific tubule segments, specific cell types and specific plasma membrane domains. Furthermore, renal epithelial cells have adapted to function in an often unique and challenging environment that includes high medullary osmolality, acidic pHs, variable blood flow and constantly changing apical and basolateral 'bathing' solutions. In this review, we focus on selected protein trafficking events by which kidney epithelial cells regulate body fluid, ion and acid-base homeostasis in response to changes in physiological conditions. We discuss aquaporin 2 and G-protein-coupled receptors in fluid and ion balance, the vacuolar H(+)-adenosine triphosphatase (V-ATPase) and intercalated cells in acid/base regulation and acidification events in the proximal tubule degradation pathway. Finally, in view of its direct role in vesicle trafficking that we outline in this study, we propose that the V-ATPase itself should, under some circumstances, be considered a fourth category of vesicle 'coat' protein (COP), alongside clathrin, caveolin and COPs.
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PMID:Sensing, signaling and sorting events in kidney epithelial cell physiology. 1917 Sep 82

Dopamine receptor, via D(1)-like and D(2)-like receptors, increases sodium excretion in kidney. We have reported positive interactions between D(3) and D(1) receptors in renal proximal tubule (RPT) cells. These reports, however do not preclude that there may be also interaction between D(3) and D(5) receptors, because of the lack of selective D(1) and D(5) receptor agonists or antagonists. We hypothesize that D(3) receptors can regulate D(5) receptors, and that D(3) receptor regulation of D(5) receptors in RPTs is impaired in spontaneously hypertensive rats (SHRs). It showed that a D(3) receptor agonist, PD128907, by the activation of protein kinase C activity, increased the expression of D(5) receptors in a concentration- and time-dependent manner in RPT cells from Wistar-Kyoto (WKY) rats. The stimulatory effect of the D(3) receptor on D(5) receptor expression was impaired in RPT cells from SHRs. The effect of D(3) receptor on D(5) receptor is functionally relevant; stimulation of D(5) receptor decreases Na(+)-K(+) adenosine triphosphatase (ATPase) activity in WKY cells. Pretreatment with D(3) receptor agonist for 24 h enhances the D(5) receptor expression and D(5) receptor-mediated inhibitory effect on Na(+)-K(+) ATPase activity in WKY cells, but decreases them in SHR cells. The effect of D(3) receptor on D(5) receptor expression and function was also confirmed in the D(5) receptor-transfected HEK293 cells. It indicates that activation of D(3) receptor increases D(5) receptor expression and function. Altered regulation of D(3) receptor on D(5) receptors may have a role in the pathogenesis of hypertension.
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PMID:D3 dopamine receptor regulation of D5 receptor expression and function in renal proximal tubule cells. 2229 82

The proximal tubule contains the highest expression of angiotensinogen mRNA and protein within the kidney and plays a vital role in the renal renin-angiotensin system. To study the regulation of angiotensinogen expression in the kidney in more detail, the proximal tubule needs to be accurately isolated from the rest of the nephron and separated into its three segments. The purpose of this study was to design a novel protocol using specific markers for the separation of proximal tubule cells into the three proximal tubule segments and to determine angiotensinogen expression in each segment. Kidneys were removed from C57BL/6J mice. The proximal tubules were aspirated from region of a Percoll gradient solution of the appropriate density. The proximal tubule was then separated into its three segments using segment-specific membrane proteins, after which each segment was characterized by a different specific marker (sodium-glucose transporter 2 for Segment 1; carbonic anhydrase IV for Segment 2; ecto-adenosine triphosphatase for Segment 3). The isolation of proximal tubules into three segments was successful, and angiotensinogen mRNA in Segment 2 and 3 and angiotensinogen protein in all three segments were confirmed. This protocol will be helpful for future studies of the detailed mechanisms of the intrarenal renin-angiotensin system.
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PMID:The establishment of a primary culture system of proximal tubule segments using specific markers from normal mouse kidneys. 2260 32

Fluorescent Ca²⁺ indicators have been essential for the analysis of Ca²⁺ signaling events in various cell types. We showed that chemical Ca²⁺ indicators, but not a genetically encoded Ca²⁺ indicator, potently suppressed the activity of Na⁺- and K⁺-dependent adenosine triphosphatase (Na,K-ATPase), independently of their Ca²⁺ chelating activity. Loading of commonly used Ca²⁺ indicators, including Fluo-4 acetoxymethyl (AM), Rhod-2 AM, and Fura-2 AM, and of the Ca²⁺ chelator BAPTA AM into cultured mouse or human neurons, astrocytes, cardiomyocytes, or kidney proximal tubule epithelial cells suppressed Na,K-ATPase activity by 30 to 80%. Ca²⁺ indicators also suppressed the agonist-induced activation of the Na,K-ATPase, altered metabolic status, and caused a dose-dependent loss of cell viability. Loading of Ca²⁺ indicators into mice, which is carried out for two-photon imaging, markedly altered brain extracellular concentrations of K⁺ and ATP. These results suggest that a critical review of data obtained with chemical Ca²⁺ indicators may be necessary.
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PMID:Fluorescent Ca²⁺ indicators directly inhibit the Na,K-ATPase and disrupt cellular functions. 2938 85

The sodium (Na⁺)/hydrogen (H⁺) exchanger 3 (NHE3) and sodium-potassium adenosine triphosphatase (Na⁺/K⁺-ATPase) are two of the most important Na⁺ transporters in the proximal tubules of the kidney. On the apical membrane side, NHE3 primarily mediates the entry of Na⁺ into and the exit of H⁺ from the proximal tubules, directly and indirectly being responsible for reabsorbing ~50% of filtered Na⁺ in the proximal tubules of the kidney. On the basolateral membrane side, Na⁺/K⁺-ATPase serves as a powerful engine driving Na⁺ out of, while pumping K⁺ into the proximal tubules against their concentration gradients. While the roles of NHE3 and Na⁺/K⁺-ATPase in proximal tubular Na⁺ transport under in vitro conditions are well recognized, their respective contributions to the basal blood pressure regulation and angiotensin II (ANG II)-induced hypertension remain poorly understood. Recently, we have been fortunate to be able to use genetically modified mouse models with global, kidney- or proximal tubule-specific deletion of NHE3 to directly determine the cause and effect relationship between NHE3, basal blood pressure homeostasis, and ANG II-induced hypertension at the whole body, kidney and/or proximal tubule levels. The purpose of this article is to review the genetic and genomic evidence for an important role of NHE3 with a focus in the regulation of basal blood pressure and ANG II-induced hypertension, as we learned from studies using global, kidney- or proximal tubule-specific NHE3 knockout mice. We hypothesize that NHE3 in the proximal tubules is necessary for maintaining basal blood pressure homeostasis and the development of ANG II-induced hypertension.
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PMID:Genetic and genomic evidence for an important role of the Na⁺/H⁺ exchanger 3 in blood pressure regulation and angiotensin II-induced hypertension. 3084 9

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