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)

Fungi normally maintain a high internal hydrostatic pressure (turgor) of about 500 kPa. In response to hyperosmotic shock, there are immediate electrical changes: a transient depolarization (1 to 2 min) followed by a sustained hyperpolarization (5 to 10 min) prior to turgor recovery (10 to 60 min). Using ion-selective vibrating probes, we established that the transient depolarization is due to Ca(2+) influx and the sustained hyperpolarization is due to H(+) efflux by activation of the plasma membrane H(+)-ATPase. Protein synthesis is not required for H(+)-ATPase activation. Net K(+) and Cl(-) uptake occurs at the same time as turgor recovery. The magnitude of the ion uptake is more than sufficient to account for the osmotic gradients required for turgor to return to its original level. Two osmotic mutants, os-1 and os-2, homologs of a two-component histidine kinase sensor and the yeast high osmotic glycerol mitogen-activated protein (MAP) kinase, respectively, have lower turgor than the wild type and do not exhibit the sustained hyperpolarization after hyperosmotic treatment. The os-1 mutant does not exhibit all of the wild-type turgor-adaptive ion fluxes (Cl(-) uptake increases, but net K(+) flux barely changes and net H(+) efflux declines) (os-2 was not examined). Both os mutants are able to regulate turgor but at a lower level than the wild type. Our results demonstrate that a MAP kinase cascade regulates ion transport, activation of the H(+)-ATPase, and net K(+) and Cl(-) uptake during turgor regulation. Other pathways regulating turgor must also exist.
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PMID:Role of a mitogen-activated protein kinase cascade in ion flux-mediated turgor regulation in fungi. 1652 3

Experiments were performed to determine the effect of plasmalemma ATPase inhibitors on cell potentials (Psi) and K(+) ((86)Rb) influx of corn root tissue over a wide range of K(+) activity. N,N'Dicyclohexylcarbodiimide (DCCD), oligomycin, and diethylstilbestrol (DES) pretreatment greatly reduced active K(+) influx and depolarized Psi at low, but not at high, K(+) activity (K degrees ). More comprehensive studies with DCCD and anoxia showed nearly complete inhibition of the active component of K(+) influx over a wide range of K degrees , with no effect on the apparent permeability constant. DCCD had no effect on the electrogenic component of the cell potential (Psi(p)) above 0.2 millimolar K degrees . Net proton efflux was rapidly reduced 80 to 90% by DCCD. Since tissue ATP content and respiration were only slightly affected by the DCCD-pretreatment, the inhibitions of active K(+) influx and Psi(p) at low K degrees can be attributed to inhibition of the plasmalemma ATPase.It is concluded that by DCCD treatment, the energy-linked electrogenic system at high K degrees is separated from the energy-linked K(+) influx system at low K degrees . The results are analyzed in terms of electrical analogue models of the membrane. The presence of two, algebraically additive electrogenic components is indicated; one is better modeled as a current source (system I) and one as a voltage source (system II). No K(+) stimulation of system II is required to produce the observed K degrees dependence of Psi(p).
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PMID:Effect of ATPase inhibitors on cell potential and k influx in corn roots. 1666 48

Net sucrose efflux from discs of fully expanded leaves of soybean (Glycine max [L.] Merr.) plants was studied to characterize sucrose efflux into the apoplast. Net sucrose efflux had a Q(10) of 2.3, was linear for at least 3.5 hours, and was selective for sucrose over glucose. Sulfhydryl group inhibitors reduced sucrose efflux by up to 80%. There was a biphasic promotion of sucrose efflux by KCl with an apparent saturable component up to about 20 millimolar, above which the effect was linear. Sucrose efflux was promoted by NaCl as a linear function of concentration. Monovalent cation ionophores did not affect sucrose efflux, regardless of external KCl concentration. Light in the absence of added HCO(3)-increased sucrose efflux by about 20%. Sucrose efflux was promoted by increasing pH from 4 to about 8, above which no additional effect was observed. When leaf discs were bathed at pH 6.0, the protonophore carbonyl cyanide m-chlorophenylhydrazone (CCCP) increased sucrose efflux by about 25%. CCCP in the presence of valinomycin had the same effect as CCCP alone. Inhibition of plasmalemma ATPase activity with N,N'-dicyclohexylcarbodiimide, diethylstilbestrol, or orthovanadate increased sucrose efflux. These data indicate that sucrose efflux from soybean leaf discs is not a result of simple leakage but is a regulated process.
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PMID:Regulation of sucrose efflux from soybean leaf discs. 1666 90

We investigated the nature of the light-induced, sodium-dependent acidification of the medium and the uptake of sodium by Synechococcus. The rate of acidification (net H(+) efflux) was strongly and specifically stimulated by sodium. The rates of acidification and sodium uptake were strongly affected by the pH of the medium; the optimal pH for both processes being in the alkaline pH range. Net proton efflux was severely inhibited by inhibitors of adenosine triphosphatase activity, energy transfer, and photosynthetic electron transport, but was not affected by the presence of inorganic carbon (C(i)). Light and C(i) stimulated the uptake of sodium, but the stimulation by C(i) was observed only when C(i) was present at the time sodium was provided. Amiloride, a potent inhibitor of Na(+)/H(+) antiport and Na(+) channels, stimulated the rate of acidification but inhibited the rate of sodium uptake. It is suggested that acidification might stem from the activity of a light dependent proton excreting adenosine triphosphatase, while sodium transport seems to be mediated by both Na(+)/H(+) antiport and Na(+) uniport.
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PMID:Nature of the light-induced h efflux and na uptake in cyanobacteria. 1666 87

The internal hydrostatic pressure (turgor) of fungal cells is maintained at 400-500 kPa. The turgor is regulated by changes in ion flux and by production of the osmotically active metabolite glycerol. In Neurospora crassa, there are at least two genetically distinct pathways that function in adaptation to hyperosmotic shock. One involves a mitogen-activated protein (MAP) kinase cascade (kinases OS-4, OS-5 and OS-2 downstream of the osmosensing OS-1); the other is less understood, but involves the cut gene, which encodes a putative phosphatase. This study examined turgor regulation, electrical responses, ion fluxes and glycerol accumulation in the cut mutant. Turgor recovery after hyperosmotic treatment was similar to that in the wild-type, for both time-course ( approximately 40 min) and magnitude. Prior to turgor recovery, the hyperosmotic shock caused a rapid transient depolarization of the membrane potential, followed by a sustained hyperpolarization that occurred concomitant with increased H(+) efflux, indicating that the plasma membrane H(+)-ATPase was being activated. These changes also occurred in the wild-type. Net fluxes of Ca(2+) and Cl(-) during turgor recovery were similar to those in the wild-type, but K(+) influx was attenuated in the cut mutant. The similar turgor recovery can be explained by the ion uptake, since glycerol did not accumulate in the cut mutant within the time frame of turgor recovery (but did accumulate in the wild-type). The results suggest that turgor regulation involves multi-faceted coordination of both ion flux and glycerol accumulation. Ion uptake is activated by a MAP kinase cascade, while CUT is required for glycerol accumulation.
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PMID:Turgor regulation in the osmosensitive cut mutant of Neurospora crassa. 1746 67

Sepsis and multiple organ failure are characterized by an excessive release of inflammatory mediators and a marked stimulation of stress hormones. These in turn have profound effects on energy and substrate metabolism: energy expenditure is generally increased, and increased lipolysis and fat oxidation are observed. Net protein breakdown occurs and leads to accelerated wasting. Most of these effects can be produced in healthy humans by administration of bacterial endotoxin or by tumor necrosis factor-alpha. Hyperlactatemia is a hallmark of sepsis and critical illness, and its severity is related to mortality. An increased lactate production, possibly secondary to activation of Na-K adenosine 5'-triphosphatase and to muscle mitochondrial dysfunction, is involved. Lactate production by immune cells and wound tissue may also play a role. Long-chain, n-3 polyunsaturated fatty acids have anti-inflammatory effects that may be beneficial in sepsis. They also decrease the stimulation of stress hormones induced by bacterial endotoxin, possibly through an effect exerted at the level of the central nervous sytem. Their use in patients with sepsis does not lead to adverse metabolic effects.
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PMID:Substrate utilization in sepsis and multiple organ failure. 1771 4

Although colonic lumen NH(4)(+) levels are high, 15-44 mM normal range in humans, relatively few studies have addressed the transport mechanisms for NH(4)(+). More extensive studies have elucidated the transport of NH(4)(+) in the kidney collecting duct, which involves a number of transporter processes also present in the distal colon. Similar to NH(4)(+) secretion in the renal collecting duct, we show that the distal colon secretory model, T84 cell line, has the capacity to secrete NH(4)(+) and maintain an apical-to-basolateral NH(4)(+) gradient. NH(4)(+) transport in the secretory direction was supported by basolateral NH(4)(+) loading on NKCC1, Na(+)-K(+)-ATPase, and the NH(4)(+) transporter, RhBG. NH(4)(+) was transported on NKCC1 in T84 cells nearly as well as K(+) as determined by bumetanide-sensitive (86)Rb-uptake. (86)Rb-uptake and ouabain-sensitive current measurement indicated that NH(4)(+) is transported by Na(+)-K(+)-ATPase in these cells to an equal extent as K(+). T84 cells expressed mRNA for the basolateral NH(4)(+) transporter RhBG and the apical NH(4)(+) transporter RhCG. Net NH(4)(+) transport in the secretory direction determined by (14)C-methylammonium (MA) uptake and flux occurred in T84 cells suggesting functional RhG protein activity. The occurrence of NH(4)(+) transport in the secretory direction within a colonic crypt cell model likely serves to minimize net absorption of NH(4)(+) because of surface cell NH(4)(+) absorption. These findings suggest that we rethink the present limited understanding of NH(4)(+) handling by the distal colon as being due solely to passive absorption.
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PMID:Ammonium transport in the colonic crypt cell line, T84: role for Rhesus glycoproteins and NKCC1. 1803 81

To test the hypothesis that colonic Na(+) transport is altered in the 5/6 nephrectomized rat model of chronic renal failure (CRF), we measured Na(+) fluxes across distal colon from control (CON), CRF, and CRF rats treated with the angiotensin II (ANG II) receptor antagonist losartan (+LOS). We also evaluated overall fluid and Na(+) balance and compared colonic protein and mRNA expression profiles for electroneutral [sodium-hydrogen exchanger (NHE)] and electrogenic Na(+) transport [epithelial sodium channel (ENaC)] in these groups. Consistent with a 60% enhancement in colonic Na(+) absorption in CRF, urinary Na(+) excretion increased by about 50% while serum Na(+) homeostasis was maintained. These CRF-induced changes in Na(+) handling were normalized by treatment with LOS. Net Na(+) absorption was also stimulated in in vitro tissues from CON rats following acute serosal addition of ANG II (10(-7) M), and this increase was blocked by AT(1) antagonism but not by an AT(2) antagonist. In CRF, colonic protein and mRNA expression variably increased for apical NHE2, NHE3, and ENaC alpha-, beta-, gamma-subunits, whereas expression of basolateral NHE1 and Na(+)-K(+)-ATPase (alpha-isoform) remained unaltered. Upregulation of the ENaC subunit mRNA was attenuated somewhat by LOS treatment. Previously, we showed that colonic AT(1) receptor protein is upregulated twofold in CRF, and here we find that AT(1) and AT(2) mRNA and AT(2) protein abundance is unchanged in CRF. We conclude that Na(+) absorption in CRF rat distal colon is increased due to elevated expression of proteins mediating electroneutral and electrogenic uptake and that it is partially mediated by AT(1) receptors.
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PMID:Increased colonic sodium absorption in rats with chronic renal failure is partially mediated by AT1 receptor agonism. 1853 92

Romanomermis culicivorax juveniles, dissected out of Aedes aegypti larvae 7 days after infection, were incubated under controlled conditions in isotonic saline containing (1)C-U-palmitic acid to investigate the nature of the transport mechanism(s) used by the nematode for transcuticular uptake of palmitic acid. Net uptake of the isotope by the nematode was of a logarithmic nature with respect to time. Uptake of palmitic acid was accomplished by a combination of diffusion and a mediated process which was substrate saturable and competitively inhibited by myristic and stearic acids. Both 2,4-dinitrophenol and ouabain inhibited uptake of palmitic acid and thus supported the hypothesis that the carrier system is of the active transport variety and is coupled to a NaK ATPase pump.
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PMID:Transport of Palmitic Acid Across the Tegument of the Entomophilic Nematode Romanomermis culicivorax. 1929 67

In the epididymis, spermatozoa acquire their ability to become motile and to fertilize an egg. A luminal acidic pH and a low bicarbonate concentration help keep spermatozoa in a quiescent state during their maturation and storage in this organ. Net proton secretion is crucial to maintain the acidity of the luminal fluid in the epididymis. A sub-population of epithelial cells, the clear cells, express high levels of the proton-pumping V-ATPase in their apical membrane and are important contributors to luminal acidification. This review describes selected aspects of V-ATPase regulation in clear cells. The assembly of a particular set of V-ATPase subunit isoforms governs the targeting of the pump to the apical plasma membrane. Regulation of V-ATPase-dependent proton secretion occurs via recycling mechanisms. The bicarbonate-activated adenylyl cyclase is involved in the non-hormonal regulation of V-ATPase recycling, following activation of bicarbonate secretion by principal cells. The V-ATPase is also regulated in a paracrine manner by luminal angiotensin II by activation of the angiotensin II type 2 receptor (AGTR2), which is located in basal cells. Basal cells have the remarkable property of extending long and slender cytoplasmic projections that cross the tight junction barrier to monitor the luminal environment. Clear cells are activated by a nitric oxide signal that originates from basal cells. Thus, a complex interplay between the different cell types present in the epithelium leads to activation of the luminal acidifying capacity of the epididymis, a process that is crucial for sperm maturation and storage.
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PMID:Regulation of luminal acidification in the male reproductive tract via cell-cell crosstalk. 1944 84


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