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)

Cardiac functions are regulated by both contractile proteins and calcium regulatory proteins. In cardiac hypertrophy, an increase in protein synthesis can be partitioned into an increase in both capacity and efficiency of synthesis. beta-cardiac myosin heavy chain (beta-MHC) isoform is predominantly expressed while alpha-MHC is suppressed in pressure overload hypertrophy. The SR Ca(2+)-ATPase is also markedly decreased in pressure overloaded hearts, while in thyrotoxic hearts both are increased. The signal transduction system in cardiac hypertrophy can be examined by stretching cardiac myocytes grown up on deformable membranes. In our analysis, stretching myocytes stimulated protein kinase C, MAP-II kinase and S6 kinase, all of which may lead to the induction of fetal-type cardiac genes and accelerated protein synthesis. Analyses of the subcellular mechanisms of cardiac hypertrophy will provide important insights into understanding of the molecular basis of heart failure.
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PMID:[Molecular basis for heart failure]. 833 89

Cardiac functions are regulated by both contractile proteins and calcium regulatory proteins. Alterations of these are considered involved in impaired contractile and diastolic functions in hypertrophied hearts. In this study, we analyzed molecular changes during the development of cardiac hypertrophy. Cardiac hypertrophy was induced by constricting the pulmonary artery in rabbits or the aorta in rats. In rabbit right ventricular hypertrophy, protein synthesis was increased to 1.8 times the control 2-4 days after pulmonary constriction. This increase in protein synthesis could be classified as an increase in both capacity and efficiency of synthesis. beta-cardiac myosin heavy chain (beta-MHC) isoform was predominantly expressed and alpha-MHC was suppressed in pressure overload hypertrophy. The switch from alpha- to beta-MHC occurred at the mRNA level. Ca(2+)-ATPase of sarcoplasmic reticulum (SR) is important because it regulates intracellular Ca2+ levels during relaxation. In pressure-overload hypertrophy, the SR Ca(2+)-ATPase was markedly decreased in both the enzyme activities and mRNA levels, while in thyrotoxic hearts both were increased. Interstitial cells also undergo phenotypic modulation which was demonstrated by the induction of nonmuscle-type MHC in pressure-overload hypertrophy. The signal transduction system in cardiac hypertrophy was examined by stretching cardiac myocytes grown on deformable membranes. In our analysis, stretching myocytes stimulated protein kinase C, MAP-II kinase and S6 kinase, all of which may lead to the induction of fetal-type cardiac genes and accelerated protein synthesis. These analyses of subcellular adaptation in cardiac hypertrophy provide important insights into understanding molecular mechanisms of cardiac functions.
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PMID:[Molecular basis for cardiac functions]. 835 May 1

Rats are generally believed to be insensitive for cardiac glycosides. However, like in humans, the hemodynamic effects may be related to the pathophysiological condition. Since the hemodynamic effects of cardiac glycosides have never been investigated in rats with heart failure, the aim of the present experiments was to investigate the role of the pathophysiological condition in the rat. Therefore, hemodynamic and cardiac effects of ouabain were investigated both in normal rats and rats with heart failure due to myocardial infarction (MI). Since the effects of ouabain may also depend on the treatment scheme, rats were treated either for a short-term period or a long-term period. Three weeks after sham surgery or ligation of the left coronary artery (MI), Wistar rats were treated for two weeks with ouabain (14.4 mg/kg.d s.c.), either continuously (osmotic minipumps) or intermittently (once daily). A separate group of rats was treated for 45-60 min (1-100 microg/kg.min ouabain; i.v. infusion 5 weeks after MI). Hemodynamic measurements were performed at rest and after volume loading in conscious rats, chronically instrumented with an electromagnetic flow probe and catheters. Induction of MI resulted in a significant increase in total peripheral resistance (TPR), and a significant decrease in basal and maximal cardiac output following volume loading (basal CO: sham, 92 +/- 5; MI, 74 +/- 5 ml/min; maximal CO: sham, 152 +/- 4; MI, 105 +/- 7 ml/min; n = 7-11). Chronic intermittent ouabain treatment further increased TPR in MI rats. In contrast, continuous ouabain treatment normalized TPR in rats. Only in continuously treated MI rats, basal and maximal CO improved significantly (basal: 83 +/- 4; maximal: 134 +/- 7 ml/min; n = 7). Acute treatment dose-dependently worsened the hemodynamic conditions of MI rats, since TPR and MAP increased and CO and stroke volume decreased significantly. These experiments demonstrate that ouabain can improve cardiac function in rats, although only in MI rats and strongly depending on the delivery regimen. Thus, in contrast to the general belief, the presently used rat model is suitable for investigation of cardiac glycosides in heart failure. The preferential improvement of cardiac function in MI rats continuously treated with ouabain may depend upon changes in Na+,K+-ATPase or altered neurohumoral conditions due to MI and chronic treatment.
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PMID:Ouabain improves cardiac function in vivo in rats with heart failure after chronic but not acute treatment. 927 26

The erythrocytic activity membrane ATPases, intraerythrocytic calcium concentration ([Ca2+]i), plasma renin activity (PRA), and angiotensin II (AT-II) in 18 essential hypertensive patients (EH) and matched normal controls were determined. In the EH group, Na(+)-K(+)-ATPase, Ca(2+)-ATPase, PRA were much lower than those in the controls, and [Ca2+]i, AT-II were higher. When blood pressure was become normotensive after a course of taking nifedipine therapy, the forementioned parameter alteration restored to approach the normal range, the changes were significnt. [Ca2+]i was positively correlated with MAP, and negatively correlated with PRA and AT-II. The results suggest that the increase erythrocytic membrane ATPase activity and decrease in renin-angiotensin system activity in nifedipine treatment may be another important antihypertensive mechanism besides accompanied with the rectifying of abnormal cellular calcium metabolism.
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PMID:[The changes of intraerythrocyte calcium metabolism and their responses to nifedipine in patients with essential hypertension]. 986 33

In Schizosaccharomyces pombe, the Wis1-Sty1 MAP (mitogen-activated protein) kinase signaling cascade is known to play a major role in cellular adaptation to adverse external stimuli, including osmotic stress, oxidative stress, nutrient deprivation, DNA-damaging agents, and heat stress. Nonetheless, it is not known whether or not this particular MAPK cascade is also involved in response to the most common stress, salinity. In this study, we provide evidence that the Wis1-Sty1 MAP cascade is implicated in salt stress response through regulating expression of a salinity-inducible gene. The downstream target gene thus identified is the cta3+ gene, which encodes a cation-transporting P-type ATPase. The salt stress-responsive nature of cta3+ expression was characterized extensively. It was found that not only the Sty1 MAP kinase but also the Atf1 transcription factor is crucial for the inducible expression of cta3+. As far as we know, this is the first instance that the stress-activated Wis1-Sty1 MAPK cascade plays a role in salt stress response in S. pombe.
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PMID:The cta3+ gene that encodes a cation-transporting P-type ATPase is induced by salt stress under control of the Wis1-Sty1 MAPKK-MAPK cascade in fission yeast. 1042 98

Activated p38gamma MAP kinase exhibited significant basal ATPase activity in the absence of a kinase substrate, and addition of a phosphoacceptor substrate increased k(cat)/K(m)20-fold. AMP-PCP was competitive with ATP binding and non-competitive with phosphoacceptor substrate binding. The nucleotide binding site affinity label 5'-(p-fluorosulfonylbenzoyl)adenosine (FSBA) bound stoichiometrically at Lys-56 in the ATP site of both unphosphorylated and activated p38gamma. AMP-PCP only protected the activated enzyme from FSBA inactivation, implying that AMP-PCP does not bind unphosphorylated p38gamma. Basal ATPase activities were also observed for activated p38alpha, ERK2 and JNK3 suggesting that the enzymatic mechanism may be similar for all classes of MAP kinases.
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PMID:Kinetic mechanism and ATP-binding site reactivity of p38gamma MAP kinase. 1056 20

Pollen tube growth depends on the differential distribution of organelles and vesicles along the tube. The role of microtubules in organelle movement is uncertain, mainly because information at the molecular level is limited. In an effort to understand the molecular basis of microtubule-based movement, we isolated from tobacco pollen tubes polypeptides that cosediment with microtubules in an ATP-dependent manner. Major polypeptides released from microtubules by ATP (ATP-MAPs) had molecular masses of 90, 80, and 41 kD. Several findings indicate that the 90-kD ATP-MAP is a kinesin-related motor: binding of the polypeptide to microtubules was enhanced by the nonhydrolyzable ATP analog AMP-PNP; the 90-kD polypeptide reacted specifically with a peptide antibody directed against a highly conserved region in the motor domain of the kinesin superfamily; purified 90-kD ATP-MAP induced microtubules to glide in motility assays in vitro; and the 90-kD ATP-MAP cofractionated with microtubule-activated ATPase activity. Immunolocalization studies indicated that the 90-kD ATP-MAP binds to organelles associated with microtubules in the cortical region of the pollen tube. These findings suggest that the 90-kD ATP-MAP is a kinesin-related microtubule motor that moves organelles in the cortex of growing pollen tubes.
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PMID:Identification and characterization of a novel microtubule-based motor associated with membranous organelles in tobacco pollen tubes. 1100 43

Stimulating cells of the mouse macrophage-like cell line RAW 264.7 with the Ca(2+)-ATPase inhibitor thapsigargin increased histamine production. Thapsigargin increased the levels of histidine decarboxylase (HDC) mRNA at 4 h and the expression of 74-kDa HDC protein at 8 h. PD98059, a specific inhibitor of MEK-1 which phosphorylates p44/p42 MAP kinase, strongly suppressed the thapsigargin-induced histamine production, the increase in HDC mRNA level and 74-kDa HDC protein expression. In contrast, SB203580, an inhibitor of p38 MAP kinase, showed only a partial inhibition of histamine production. TPA and LPS also induced histamine production in RAW 264.7 cells, and the histamine production induced by TPA or LPS was also inhibited by PD98059, but the effect of SB203580 was partial. The synthetic glucocorticoid dexamethasone inhibited thapsigargin-induced histamine production, 74-kDa HDC protein expression and the activation of p44/p42 MAP kinases. In conclusion, the increase in histamine production in macrophages stimulated with inflammatory stimulants is due to the increased expression of 74-kDa HDC, which is positively regulated by activated p44/p42 MAP kinases. Dexamethasone inhibits thapsigargin-induced HDC protein expression and histamine production by inhibiting the MAP kinase activation.
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PMID:[Regulation of histamine production in macrophages]. 1149 23

Steroids administrated antenatally to the mothers improve postnatal outcomes of the newborns with pleiotropic effects. Furthermore steroids have been used in preterm infants to prevent or treat chronic lung disease. Synthetical glucocorticoids readily cross placental barrier and reach significant pharmacologic levels in the fetus: besides their well known pulmonary effects they have a concomitant maturational effect of postnatal renal function in preterm infants both with a direct and indirect effect. Endogenous and exogenous glucocorticoids play a role in the maintenance of glomerular filtration (GFR). The antenatal administration of steroids increases the GFR, in association to the maturation of the tubular function. According to different studies the improvement of renal function, expressed by the increase of GFR, is only partially referable to the increase of MAP and the improvement of the cardiovascular status, while it was imputable to a direct renal effect of the steroids, especially on the renal blood flow, on functional glomerular surface area available for filtration and on the glomerular filtrate of the single cortical nephron. However debate remains about the mechanism through which steroids would act on the renal vascular smooth muscolature. The increase the GFR observed after the antenatal administration of glucocorticoids in premature fetuses is also accompanied by an increase of urinary flow and of fractional excretion of sodium. Glucocorticoids would increase the proximal reabsorption of sodium increasing directly the function and the expression of the sodium transporters and both indirectly and directly increasing the activity of Na-K-ATPase. In extremely low weight antenatal administration of betamethasone or dexamethasone was associated with lower estimated insensible water loss, secondary to a direct maturational effect in the skin epithelial barrier, as well as an increased reabsorption of the fetal lung fluid. Moreover antenatal glucocorticoid administration was associated, at birth, to a significant suppression of plasma renin activity and angiotensin II in comparison to the controls. Despite the wide use of the steroidal therapy in the prevention of the bronchopulmonary dysplasia, only few articles, in literature, analyse the effects of glucocorticoids on postnatal renal function, such as the increase in urinary flow. The authors think that steroids contribute in a meaningful way to the clinical improvement observed in children with BPD through the maturative action on the premature kidney with effect both at glomerular and tubular level.
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PMID:Renal effects of antenatally or postnatally administered steroids. 1198 24

Bone resorption is glucose concentration dependent. Mechanisms regulating glucose-dependent increases in bone resorption have not been identified. Glucose activates p38 MAP-kinase in other cells and since MAP kinases activate transcription factors, we hypothesized that glucose-stimulated bone resorption may be modulated by increased expression of the vacuolar H(+)-ATPase. Glucose activates osteoclast p38 MAP-kinase in a time and concentration-dependent manner as determined by Western analysis with phospho-specific p38 antibody while total p38 levels are unchanged. The K0.5 for glucose-dependent activation of p38 MAP-kinase is approximately 7 mM, activation is maximal at 30 min and is elevated but returning to basal levels by 60 min. The concentration-dependent increase in H(+)-ATPase expression was confirmed by Northern analysis. The specific inhibitor of p38 MAP-kinase, SB203580, inhibited glucose transport in osteoclasts, as well as glucose concentration-dependent increases in bone resorption and expression of H(+)-ATPase A and B subunits. Glucose had no effect on calmodulin expression levels that are regulated in response to other environmental changes. The glucose-stimulated increase in H(+)-ATPase mRNA expression is a specific response to glucose since glucose has little effect on G3PDH mRNA levels. We conclude that glucose regulates osteoclast H(+)-ATPase expression by a mechanism likely to involve p38 MAP-kinase.
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PMID:Glucose-dependent regulation of osteoclast H(+)-ATPase expression: potential role of p38 MAP-kinase. 1221 Jul 24


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