Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of intraventricular injection of kainic acid on the Na,K-ATPase (Na,K pump) were examined in discrete pyramidal cell regions of rat hippocampus. [3H]Ouabain binding was used to quantitate Na,K-ATPase catalytic subunits and in situ hybridization was used to determine Na,K-ATPase mRNA levels. Large decreases were found in both [3H]ouabain binding and alpha 3 isoform mRNA in hippocampus areas, especially in the CA3 pyramidal cell layer, which sustains heavy cell losses as a result of bilateral, intraventricular injection of kainic acid. Substantial decreases in the high affinity component of ouabain binding and in the alpha 3 isoform mRNA (but not isoforms for other Na,K-ATPase subunits) were also observed in the CA1 region of hippocampus, an area preserved in this model. High affinity [3H]ouabain binding was decreased 25-33% in the stratum pyramidale and stratum radiatum after treatment with kainic acid, and alpha 3 mRNA was decreased by 26-50%. To further characterize the decrease in alpha 3 mRNA, animals were killed at 1, 2, and 3 weeks after injection of kainate and results show a large decrease in alpha 3 mRNA only at 2 weeks recovery time. While the pathology underlying temporal lobe epilepsy is unclear, changes in the Na,K-ATPase may be involved in abnormal firing characteristics of cells in epileptic tissue.
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PMID:Na,K-ATPase is decreased in hippocampus of kainate-lesioned rats. 801 44

NaCl regulation of plasma membrane H(+)-ATPase gene expression in the glycophyte tobacco (Nicotiana tabacum L. var Wisconsin 38) and the halophyte Atriplex nummularia L. was evaluated by comparison of organ-specific mRNA abundance using homologous cDNA probes encoding the ATPases of the respective plants. Accumulation of mRNA was induced by NaCl in fully expanded leaves and in roots but not in expanding leaves or stems. The NaCl responsiveness of the halophyte to accumulate plasma membrane H(+)-ATPase mRNA in roots was substantially greater than that of the glycophyte. Salt-induced transcript accumulation in A. nummularia roots was localized by in situ hybridization predominantly to the elongation zone, but mRNA levels also increased in the zone of differentiation. Increased message accumulation in A. nummularia roots could be detected within 8 h after NaCl (400 mM) treatment, and maximal levels were severalfold greater than in roots of untreated control plants. NaCl-induced plasma membrane H(+)-ATPase gene expression in expanded leaves and roots presumably indicates that these organs require increased H(+)-electrochemical potential gradients for the maintenance of plant ion homeostasis for salt adaptation. The greater capacity of the halophyte to induce plasma membrane H(+)-ATPase gene expression in response to NaCl may be a salt-tolerance determinant.
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PMID:NaCl regulation of plasma membrane H(+)-ATPase gene expression in a glycophyte and a halophyte. 802 33

The regulation of cytosolic Ca2+ concentration during excitation-contraction coupling is altered in the failing human heart. Previous studies have focused on disturbances in Ca2+ release and reuptake from the sarcoplasmic reticulum (SR), whereas functional studies of the cardiac Na(+)-Ca2+ exchanger, another important determinant of myocyte homeostasis, are lacking for the failing human heart. Using a cardiac Na(+)-Ca2+ exchanger cDNA recently cloned from a guinea pig cDNA library, we investigated the gene expression of the cardiac Na(+)-Ca2+ exchanger in relation to the SR Ca(2+)-ATPase. Expression of both genes was quantified in left ventricular myocardium from 24 failing human cardiac explants and 7 control heart samples in relation to beta-myosin heavy chain mRNA by slot blot analysis. Compared with patients with nonfailing hearts, patients with dilated cardiomyopathy (DCM, n = 13) showed a 55% increase in Na(+)-Ca2+ exchanger mRNA levels (P < .05 versus control value) and a 41% increase in patients with coronary artery disease (CAD, n = 11). In the same hearts, SR Ca(2+)-ATPase mRNA levels were decreased by 50% in DCM and by 45% in CAD (P < .05 for both versus control value). There was a positive correlation between Na(+)-Ca2+ exchanger and SR Ca(2+)-ATPase mRNA levels both in normal and failing human hearts, albeit with different slopes and intercepts of the regression line. The Na(+)-Ca2+ exchanger protein levels as assessed by Western blot analysis and normalized to beta-myosin heavy chain protein were increased in DCM and CAD (P < .05 and P < .01 versus control value, respectively), whereas SR Ca(2+)-ATPase protein levels were reduced (P < .05 for both groups versus control values). Thus, the Na(+)-Ca2+ exchanger gene expression is enhanced in failing human hearts and may, in part, compensate for the depressed SR function with regard to diastolic Ca2+ removal.
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PMID:Gene expression of the cardiac Na(+)-Ca2+ exchanger in end-stage human heart failure. 806 18

Glucocorticoids modulate the maturation of Na(+)-K(+)-ATPase mRNA in a tissue- and age-dependent manner. In this study, we report the effect of glucocorticoids on Na(+)-K(+)-ATPase gene transcription in the infant rat kidney. Ten-day-old rats were treated with one intraperitoneal injection of betamethasone. In glucocorticoid-treated rats, there was a significant increase in renal cortical alpha 1- and beta 1-mRNAs (3.08 +/- 0.34- and 4.06 +/- 0.10-fold). Pretreatment with cycloheximide, an inhibitor of protein synthesis, did not abolish the increase in alpha 1- and beta 1-mRNA after glucocorticoids. The alpha 1- and beta 1-gene transcription rates were significantly increased in nuclei isolated from kidneys of glucocorticoid-treated rat (2.16 +/- 0.05- and 3.12 +/- 0.50-fold). Interaction between nuclear proteins and Na(+)-K(+)-ATPase alpha 1-promoter was studied by gel retardation assay. Nuclear protein from glucocorticoid-treated rats retarded a fragment of alpha 1-promoter that includes a half-consensus glucocorticoid response element (GRE) at position -750 bp but did not retard a fragment including a half-consensus GRE at position -481. Retardation of alpha 1-promoter was inhibited by incubation with molar excess of GRE or with a monoclonal antibody against glucocorticoid receptor. We conclude that in the infant kidney, glucocorticoids directly stimulate the transcription of alpha 1- and beta 1-Na(+)-K(+)-ATPase subunits. It is likely that the binding of glucocorticoid receptor to alpha 1-Na(+)-K(+)-ATPase promoter requires the presence of an auxiliary factor.
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PMID:Glucocorticoids regulate the transcription of Na(+)-K(+)-ATPase genes in the infant rat kidney. 807 80

The H(+)-K(+)-adenosinetriphosphatase (ATPase) is expressed in the parietal cell and is responsible for acid secretion by the stomach. Histamine binds to an H2 receptor and activates adenylate cyclase and intracellular calcium concentration ([Ca2+]i) elevation, stimulating acid secretion. It has been shown that omeprazole administered to rats increases serum gastrin and transiently increases the level of mRNA for the alpha-subunit of the pump, but this increase is blocked by the presence of the H2-receptor antagonist, famotidine [A. Tari, G. Yamamoto, K. Sumii, M. Sumii, Y. Takehara, K. Haruma, G. Kajiyama, V. Wu, G. Sachs, and J. H. Walsh. Am. J. Physiol. 265 (Gastrointest. Liver Physiol. 28): G752-G758, 1993]. These observations suggest that the release of histamine induced by gastrin is essential for the increase of the expression of mRNA induced by omeprazole. Infusion of histamine at 15 mumol.kg-1.h-1 i.v. for 1 h increased the alpha-subunit mRNA level by 144 +/- 2.4% and induced a stimulated morphological appearance of the parietal cell. These changes were inhibited completely by the competitive H2-receptor antagonist famotidine, which elevated gastric pH and serum gastrin. Famotidine also reduced the level of H(+)-K(+)-ATPase mRNA compared with control animals. No change in the expression of beta-actin mRNA was observed in any group of animals. These data provide direct evidence for histamine stimulation of H(+)-K(+)-ATPase alpha-subunit gene expression by activation of the H2 receptor.
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PMID:Effect of histamine on rat gastric H(+)-K(+)-ATPase alpha-subunit expression. 816 83

The yeast plasma membrane H(+)-ATPase generates a membrane electrochemical gradient which is required for the secondary uptake of nutrients. Although the ATPase has previously been shown to be post-translationally regulated in response to the availability of glucose, there has been no evidence to date for transcriptional regulation of the ATPase gene (PMA1). In this work, we have examined the pool of newly synthesized ATPase that accumulates in secretory vesicles en route to the cell surface in the temperature-sensitive secretory mutant sec6-4, and have observed changes in the level of ATPase polypeptide as a function of the glucose concentration in the growth medium. In parallel, there were rapid and reversible changes in the levels of ATPase mRNA. Finally, when cells were grown on a variety of carbon sources, the amount of ATPase polypeptide was proportional to the specific growth rate, suggesting that PMA1 expression is adjusted according to the metabolic state of the cell. These results complement the findings of Capieaux et al. (Capieaux, E., Vignais, M.-L., Sentenac, A. and Goffeau, A. (1989). J. Biol. Chem. 264, 7437-7446), who show that the transcriptional factor TUF/RAP1 binds to upstream activating sequences in the PMA1 gene. Taken together, the results suggest a model in which transcriptional regulation of the ATPase gene by glucose is mediated by TUF/RAP1.
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PMID:Transcriptional regulation by glucose of the yeast PMA1 gene encoding the plasma membrane H(+)-ATPase. 825 14

We studied Na,K-ATPase mRNA expression in cardiomyopathic (Bio 14.6) and normal (F1b) Syrian hamster ventricles. In Northern blot analysis, Na,K-ATPase alpha 1, alpha 2, alpha 3 and beta 1 isoform mRNAs were detected in 3-week-old Bio 14.6 and F1b hamster ventricles. We then investigated the expression of alpha 1 subunit mRNA in Bio 14.6 hamster ventricles at the ages of 3 weeks prehypertrophic and 30 weeks hypertrophic, and in age-matched F1b hamster ventricles. The alpha 1 subunit mRNA levels in Bio 14.6 hamster ventricles were approximately 50% lower than those in F1b hamster ventricles at both 3 and 30 weeks of age. Na,K-ATPase activity measured in membrane fractions from the ventricles of 3-week-old Bio 14.6 hamsters was also approximately 20% lower than that of F1b hamsters, suggesting that the differences in the mRNA level were associated with the differences in the protein level. We conclude that Na,K-ATPase mRNA expression and enzyme activity are significantly decreased in the hearts of Bio 14.6 hamsters even before the onset of hypertrophy and cardiomyopathy, suggesting that the altered expression of Na,K-ATPase gene is an early event in the pathogenesis of cardiomyopathy in this animal model.
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PMID:Decreased Na,K-ATPase gene expression in cardiomyopathic hamster hearts. 827 20

The postnatal maturation of Na+,K(+)-ATPase alpha- and beta-subunit genes can be accelerated in the rat kidney by the administration of glucocorticoid hormones (GC). In heart, Na+,K(+)-ATPase alpha-isoform and beta-subunit genes exhibit a complex pattern of expression during development. This study examines the role of GC in the regulation of Na+,K(+)-ATPase mRNA abundance in rat heart during infancy. In 10-d-old rats given injections with a single intraperitoneal dose of betamethasone or diluent, the Na+,K(+)-ATPase activity was 2-fold higher in treated than in control rats after 24 h. GC differentially regulated the mRNA for Na+,K(+)-ATPase subunits. A significant increase in Na+,K(+)-ATPase mRNA occurred with a dose of 2.5 micrograms betamethasone/100 g body weight. The following experiments were performed with a saturating dose of 60 micrograms betamethasone/100 g body weight. The alpha 1 mRNA was moderately but significantly increased (1.5-fold) 6 h after treatment. The mRNA for the alpha 2 subunit increased 2.2-fold after betamethasone treatment. The mRNA for beta 1 was numerically increased after 20 min (1.3-fold); it was 1.5-fold higher (p < 0.05) after 1 h and was 3-fold higher after 6 h (p < 0.01). Betamethasone treatment did not significantly change the abundance of the mRNA for the alpha 3 subunit. The expression of actin mRNA was not altered after GC. These data indicate that GC hormones may act as a "molecular switch" in the developmental expression of the mRNA for the Na+,K(+)-ATPase alpha-isoforms and contribute in stimulating the maturation of rat heart during the preweaning period.
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PMID:Glucocorticoids differentially regulate the mRNA for Na+,K(+)-ATPase isoforms in infant rat heart. 838 51

We have previously reported that in the infant rat renal cortex, a saturating dose of glucocorticoid hormones (GC) rapidly increases the abundance of Na+,K(+)-ATPase mRNA. We now show that this effect is dose dependent. In the renal cortex of 10-d-old rats, an increase in renal Na+,K(+)-ATPase mRNA occurs with 2.5 micrograms betamethasone/100 g body weight. In subsequent experiments, performed 6 h after a saturating dose (60 micrograms/100 g body weight), we show that the effect is age dependent. The most marked effects on renal cortical alpha-mRNA were found at 10 d of age (5.3- +/- 0.9-fold). A significant increase was also found in 20-d-old rats (1.6- +/- 0.2-fold), but no effect was found in fetal and 5-d-old rats. Studies were also performed on the lung, where the most marked effect was noted in the perinatal period (2.0- +/- 0.1-fold 2 d before birth and 1.76 +/- 0.2 at 5 d of age), but no effect on alpha-mRNA was found at 10 and 20 d. In one protocol, the effect of betamethasone on renal Na+K(+)-ATPase mRNAs abundance was determined in adult adrenalectomized rats. In these rats, betamethasone induced a significant 1.6- +/- 0.2-fold and 1.8- +/- 0.3-fold increase in renal Na+,K(+)-ATPase mRNA. This effect, however, was significantly smaller than the increase induced in intact 10-d-old rats. GC induction of Na+,K(+)-ATPase mRNA is age and tissue dependent and is dependent on factors other than GC-receptor availability. The GC-sensitive period appears to coincide with the physiologic need for organ maturation.
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PMID:Sensitive periods for glucocorticoids' regulation of Na+,K(+)-ATPase mRNA in the developing lung and kidney. 838 52

We examined the effect of a high-salt (HS) diet on the regulation of renal cortical Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) in young Dahl salt-sensitive (DS) and salt-resistant (DR) rats. The activity of Na(+)-K(+)-ATPase, determined in permeabilized proximal tubule segments, was similar in DS and DR rats on normal salt (NS) diet. HS diet resulted in a twofold increase in proximal tubule Na(+)-K(+)-ATPase activity in DS rats but not in DR rats. The mRNA abundance, which was also similar in DS and DR rats on NS diet, increased after 2 days on HS diet in both innervated and denervated kidneys from DS rats but had no effect in DR rats. The activity of Na(+)-K(+)-ATPase and the content of alpha 1- and beta-protein in cortical homogenate were similar in DS and DR rats on both NS and HS diets. Treatment with benserazide, an inhibitor of dopa decarboxylase, upregulated proximal tubule Na(+)-K(+)-ATPase activity and increased Na(+)-K(+)-ATPase mRNA in DR rats on HS diet. Taken together, these data indicate that there is a primary defect in the dynamic hormonal regulation of Na(+)-K(+)-ATPase activity in intact tubular cells, which might stimulate Na(+)-K(+)-ATPase transcription.
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PMID:High-salt diet upregulates activity and mRNA of renal Na(+)-K(+)-ATPase in Dahl salt-sensitive rats. 838 12


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