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 basal membrane potential (V(b)) of Locusta Malpighian tubule cells in control saline results from its relatively high permeability to potassium. In the presence of 1 mM barium added to the control saline V(b) hyperpolarized from a mean resting potential of -72.1 mV to -90.1 mV. On substituting rubidium for potassium in the control saline, V(b) also hyperpolarized to a value of -91.4 mV. Rubidium was also similarly effective in hyperpolarizing the basal membrane even in the presence of control concentrations of potassium in the bathing medium. Substitution of rubidium for potassium also effected a approximately 50% reduction in the rate of fluid secretion. The action of inhibitors on V(b) in the presence of rubidium showed that V(b) under these conditions probably originated from the bafilomycin-sensitive electrogenic potential generated across the apical membrane by a V-type ATPase. The responses of V(b) to potassium, barium and rubidium and their inhibition of fluid secretion suggest the presence of a substantial rubidium-blockable potassium conductance located on the basal membrane of Locusta Malpighian tubule cells.
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PMID:Rubidium reduces potassium permeability and fluid secretion in Malpighian tubules of Locusta migratoria, L. 1124 52

The role of angiotensin subtype-1 (AT1) and -2 (AT2) receptors in mediating the effects of angiotensin II (ANG II) on several K+ transporters was studied in rat distal colon using an Ussing chamber. Angiotensin II induced K+ secretion at two different doses. Secretion occurred at 10-(8) and 10-(4) M, as a result of an increase in serosal-to-mucosal flux (Js-m). The ANG II-induced stimulation of Js-m at a low dose (10-(8) M) was abolished by PD123319 while losartan did not alter the low-dose ANG II-dependent increase in Js-m. In contrast, the increase in Js-m induced by a high-dose of ANG II (10-(4) M) was blocked by losartan, whereas PD123319 partially reduced the stimulatory effect. In the presence of both blockers, high-dose ANG II induced an inhibition of basal Js-m. Low-dose ANG II activated the barium-sensitive K+ channels, whereas the Na+, K+, 2Cl- cotransporter and the Na+, K+ -ATPase pump were unchanged. At the high dose, ANG II activated the barium-sensitive K+ channels and the Na+, K+, 2Cl- cotransporter and inhibited the Na+, K+ -ATPase pump. These data indicate that ANG II stimulates serosal-to-mucosal K+ flux in the rat distal colon at high and low doses via different receptors and K+ transporters.
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PMID:Regulation of K+ transport in the rat distal colon via angiotensin II subtype receptors and K+ -pathways. 1135 Feb 74

Outer sulcus epithelial cells were recently found to actively reabsorb cations from the cochlear luminal fluid, endolymph, via nonselective cation channels in the apical membrane. Here we determined the transport properties of the basolateral membrane with the whole-cell patch clamp technique; the apical membrane contributed insignificantly to the recordings. Outer sulcus epithelial cells exhibited both outward and inward currents and had a resting membrane potential of -90.4 +/- 0.7 mV (n = 78), close to the Nernst potential for K+ (-95 mV). The reversal potential depolarized by 54 mV for a tenfold increase in extracellular K+ concentration with a K+/Na+ permeability ratio of 36. The most frequently observed K+ current was voltage independent over a broad range of membrane potentials. The current was reduced by extracellular barium (10-5 to 10-3 m), amiloride (0.5 mm), quinine (1 mm), lidocaine (5 mm) and ouabain (1 mm). On the other hand, TEA (20 mm), charybdotoxin (100 nm), apamin (100 nm), glibenclamide (10 microm), 4-aminopyridine (1 mm) and gadolinium (1 mm) had no significant effect. These data suggest that the large K+ conductance, in concert with the Na+,K+-ATPase, of the basolateral membrane of outer sulcus cells provides the driving force for cation entry across the apical membrane, thereby energizing vectorial cation absorption by this epithelium and contributing to the homeostasis of endolymph.
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PMID:Basolateral K+ conductance establishes driving force for cation absorption by outer sulcus epithelial cells. 1171 47

The present study compared ouabain-sensitive unidirectional K+ flux into (JinK) and out of (JoutK) perfused rat hindlimb skeletal muscle in situ and mouse flexor digitorum brevis (FDB) in vitro. In situ, 5 mM ouabain inhibited 54 +/- 4% of the total JinK in 28 +/- 1 min, and increased the net and unidirectional efflux of K+ within 4 min. In contrast, 1.8 mM ouabain inhibited 40 +/- 8% of the total JinK in 38 +/- 2 min, but did not significantly affect JoutK. In vitro, 1.8 and 0.2 mM ouabain decreased JinK to a greater extent (83 +/- 5%) than in situ, but did not significantly affect 42K loss rate compared with controls. The increase in unidirectional K+ efflux (JoutK) with 5 mM ouabain in situ was attributed to increased K+ efflux through cation channels, since addition of barium (1 mM) to ouabain-perfused muscles returned JoutK to baseline values within 12 min. Perfusion with 5 mM ouabain plus 2 mM tetracaine for 30 min decreased JinK 46 +/- 9% (0.30 +/- 0.03 to 0.16 +/- 0.02 micromol x min(-1) x g(-1)), however tetracaine was unable to abolish the ouabain-induced increase in unidirectional K+ efflux. In both rat hindlimb and mouse FDB, tetracaine had no effect on JoutK. Perfusion of hindlimb muscle with 0.1 mM tetrodotoxin (TTX, a Na+ channel blocker) decreased JinK by 15 +/- 1%, but had no effect on JoutK; subsequent addition of ouabain (5 mM) decreased JinK a further 32 +/- 2%. The ouabain-induced increase in unidirectional K+ efflux did not occur when TTX was perfused prior to and during perfusion with 5 mM ouabain. We conclude that 5 mM ouabain increases the unidirectional efflux of K+ from skeletal muscle through a barium and TTX-sensitive pathway, suggestive of voltage sensitive Na+ channels, in addition to inhibiting Na+/K+-ATPase activity.
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PMID:Ouabain stimulates unidirectional and net potassium efflux in resting mammalian skeletal muscle. 1176 95

Proteinase-activated receptor (PAR) type 2 (PAR-2) has been shown to mediate ion secretion in cultured epithelial cells and rat jejunum. With the use of a microUssing chamber, we demonstrate the role of PAR-2 for ion transport in native human colonic mucosa obtained from 30 normal individuals and 11 cystic fibrosis (CF) patients. Trypsin induced Cl(-) secretion when added to the basolateral but not luminal side of normal epithelia. Activation of Cl(-) secretion by trypsin was inhibited by indomethacin and was further increased by cAMP in normal tissues but was not present in CF colon, indicating the requirement of luminal CF transmembrane conductance regulator. Effects of trypsin were largely reduced by low Cl(-), by basolateral bumetanide, and in the presence of barium or clotrimazole, but not by tetrodotoxin. Furthermore, trypsin-induced secretion was inhibited by the Ca(2+)-ATPase inhibitor cyclopiazonic acid and in low-Ca(2+) buffer. The effects of trypsin were almost abolished by trypsin inhibitor. Thrombin, an activator of PAR types 1, 3, and 4, had no effects on equivalent short-circuit currents. The presence of PAR-2 in human colon epithelium was confirmed by RT-PCR and additional experiments with PAR-2-activating peptide. PAR-2-mediated intestinal electrolyte secretion by release of mast cell tryptase and potentiation of PAR-2 expression by tumor necrosis factor-alpha may contribute to the hypersecretion observed in inflammatory processes such as chronic inflammatory bowel disease.
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PMID:Activation of ion secretion via proteinase-activated receptor-2 in human colon. 1180 40

The contributions of Na+/K+-ATPase, K+ channels, and the NaK2Cl cotransporter (NKCC) to total and unidirectional K+ flux were determined in mammalian skeletal muscle at rest. Rat hindlimbs were perfused in situ via the femoral artery with a bovine erythrocyte perfusion medium that contained either 86Rb or 42K, or both simultaneously, to determine differences in ability to trace unidirectional K+ flux in the absence and presence of K+-flux inhibitors. In most experiments, the unidirectional flux of K+ into skeletal muscle (J(in)K) measured using 86Rb was 8-10% lower than J(in)K measured using 42K. Ouabain (5 mM) was used to inhibit Na+/K+-ATPase activity, 0.06 mM bumetanide to inhibit NKCC activity, 1 mM tetracaine or 0.5 mM barium to block K+ channels, and 0.05 mM glybenclamide (GLY) to block ATP-sensitive K+ (K(ATP)) channels. In controls, J(in)K remained unchanged at 0.31 +/- 0.03 micromol x g(-1) x min(-1) during 55 min of perfusion. The ouabain-sensitive Na+/K+-ATPase contributed to 50 +/- 2% of basal J(in)K, K+ channels to 47 +/- 2%, and the NKCC to 12 +/- 1%. GLY had minimal effect on J(in)K, and both GLY and barium inhibited unidirectional efflux of K+ (J(out)K) from the cell through K+ channels. Combined ouabain and tetracaine reduced J(in)K by 55 +/- 2%, while the combination of ouabain, tetracaine, and bumetanide reduced J(in)K by 67 +/- 2%, suggesting that other K+-flux pathways may be recruited because the combined drug effects on inhibiting J(in)K were not additive. The main conclusions are that the NKCC accounted for about 12% of J(in)K, and that K(ATP) channels accounted for nearly all of the J(out)K, in resting skeletal muscle in situ.
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PMID:An integrative, in situ approach to examining K+ flux in resting skeletal muscle. 1182 43

We characterized MLL3, a new human member of the TRX/MLL gene family. MLL3 is expressed in peripheral blood, placenta, pancreas, testes, and foetal thymus and is weakly expressed in heart, brain, lung, liver, and kidney. It encodes a predicted protein of 4911 amino acids containing two plant homeo domains (PHD), an ATPase alpha_beta signature, a high mobility group, a SET (Suppressor of variegation, Enhancer of zeste, Trithorax) and two FY (phenylalanine tyrosine)-rich domains. The amino acid sequence of the SET domain was used to obtain a phylogenetic tree of human MLL genes and their homologues in different species. MLL3 is closely related to human MLL2, Fugu mll2, a Caenorhabditis elegans predicted protein, and Drosophila trithorax-related protein. Interestingly, PHD and SET domains are frequently found in proteins encoded by genes that are rearranged in different haematological malignancies and MLL3 maps to 7q36, a chromosome region that is frequently deleted in myeloid disorders. Partial duplications of the MLL3 gene are found in the juxtacentromeric region of chromosomes 1, 2, 13, and 21.
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PMID:MLL3, a new human member of the TRX/MLL gene family, maps to 7q36, a chromosome region frequently deleted in myeloid leukaemia. 1189 Oct 48

Beside its well-known role in bone development, vascularization plays a major role in bone cell migration for bone remodeling and metastatic tumor invasion. However, the various techniques used to identify vessels in bone have never been tested for trabecular bone vessel quantification, whereas bone remodeling quantitative parameters are commonly assessed. In this context, we developed and compared various histological techniques used to visualize blood vessels in rat bone in order to quantify them. First, several products were tested by intracardiac infusion to opacify the bone vascular network. The best results were obtained using either an India ink-1% agarose solution or an India ink-saturated barium sulfate solution followed by X-ray microradiography. Second, to identify the types of vessels, we also performed histoenzymology and immunohistochemistry stainings. Neither alkaline phosphatase (for endothelial cells) nor adenosine triphosphatase (ATPase) stainings (for smooth muscle cells) provided a low enough background to allow for vessel identification and quantification. For immunohistochemistry, various specific vessel constituents were analyzed: laminin, smooth muscle cell alpha-actin, factor VIII, and lectin Griffonia simplifolia. Anti-laminin and anti-smooth muscle cell alpha-actin antibodies gave the best results for quantification. Third, after optimization of these techniques, we performed quantitative bone and vessel histomorphometry on two groups of 12 rats each, for which bone remodeling and vessel number and area parameters were measured. No statistical differences were observed between the two groups, confirming the reproducibility of our measurements. A significant relationship was found between vessel number and histodynamic parameters; that is, bone formation rate correlated positively with India ink-positive vessel area (p < 0.009, r2 = 0.54) and alpha-actin-positive vessel number (p < 0.05, r2 = 0.66). Furthermore, we report reproducible techniques for visualization and quantification of vessels in bone that also allowed for simultaneous conventional bone histomorphometry. This methodology should help researchers to better understand the functional and anatomical relationship between trabecular bone and its vascularization during normal or pathological processes.
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PMID:Relationships between trabecular bone remodeling and bone vascularization: a quantitative study. 1193 53

The effect of trichloroethanol (TCEt), the active metabolite of chloral hydrate, on the intracellular concentration of calcium ([Ca(2+)](i)) was investigated in rat submandibular glands (RSMG) acini loaded with fura-2. TCEt (1 - 10 mM) increased the [Ca(2+)](i) independently of the presence of calcium in the extracellular medium. Dichloroethanol (DCEt) and monochloroethanol (MCEt) reproduced the stimulatory effect of TCEt but at much higher concentrations (about 6 fold higher for DCEt and 20 fold higher for MCEt). TCEt mobilized an intracellular pool of calcium, which was depleted by a pretreatment with thapsigargin, an inhibitor of the sarcoplasmic and endoplasmic reticulum calcium-dependent ATPases, but not with FCCP, an uncoupler of mitochondria. TCEt 10 mM inhibited by 50% the thapsigargin-sensitive microsomal Ca(2+)-ATPase. DCEt 10 mM and MCEt 10 mM inhibited the ATPase by 20 and 10%, respectively. TCEt inhibited the increase of the [Ca(2+)](i) and the production of inositol phosphates in response to carbachol, epinephrine and substance P. TCEt inhibited the uptake of calcium mediated by the store-operated calcium channel (SOCC). ATP and Bz-ATP increased the [Ca(2+)](i) in RSMG acini and this effect was blocked by extracellular magnesium, by Coomassie blue and by oxydized ATP (oATP). TCEt potentiated the increase of the [Ca(2+)](i) and of the uptake of extracellular calcium in response to ATP and Bz-ATP. TCEt had no effect on the uptake of barium and of ethidium bromide in response to purinergic agonists. These results suggest that TCEt, at sedative concentrations, exerts various effects on the calcium regulation: (1) it mobilizes a thapsigargin-sensitive intracellular pool of calcium in RSMG acini; (2) it inhibits the uptake of calcium via the SOCC; (3) it inhibits the activation by G protein-coupled receptors of a polyphosphoinositide-specific phospholipase C. It does not interfere with the activation of the ionotropic P2X receptors. The use of chloral hydrate should be avoided in studies exploring the in vivo responses to sialagogues.
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PMID:Multiple effects of trichloroethanol on calcium handling in rat submandibular acinar cells. 1205 35

This study tested the hypothesis that the NKCC is involved in volume regulation, specifically regulatory volume increase (RVI), in resting skeletal muscle. Neurally and vascularly isolated rat hindlimbs were perfused with a bovine erythrocyte perfusate containing (42)K or (86)Rb as markers of unidirectional K(+) flux across the sarcolemma. Compared to controls, perfusion with 120 microM bumetanide (a specific inhibitor of the NKCC) decreased J(in)K by 15+/-2%, indicating the functional presence of the NKCC. Experiments with ouabain (to block active K(+) transport by the Na,K ATPase) showed that the bumetanide-sensitive component of J(in)K comprised 35% of the total ouabain-sensitive J(in)K. Inhibition of NKCC resulted in a net loss of water by muscle. When hindlimbs were perfused with hypertonic (380 mOsm/L by addition of sucrose) perfusate for 20 min, after initially blocking K(+) channels with 1 mM barium, J(in)K rapidly (2-3 min) increased 2-fold followed by a rapid decline. This rapid, transient increase in J(in)K was abolished with bumetanide, confirming that perfusion with hypertonic perfusate stimulated NKCC activity and RVI. The hypertonic perfusate also resulted in temporally associated decreases in net water uptake by muscle. It is concluded that a functional NKCC is present in mammalian skeletal muscle and that it is involved in cell volume regulation.
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PMID:K(+) transport and volume regulatory response by NKCC in resting rat hindlimb skeletal muscle. 1243 64


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