Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To characterize the interaction of insulin with the renal proximal tubular cell, we measured insulin-stimulated phosphorylation in basolateral membranes and brush border membranes isolated from canine renal cortex. Insulin stimulated the specific phosphorylation of a 92,000 Mr protein band demonstrable on autoradiograms of sodium dodecyl sulfate-polyacrylamide gels of basolateral membranes. Dephosphorylation of the 92,000 Mr band occurred over time. Insulin-stimulated phosphorylation was concentration dependent, being clearly detectable at 10(-9) M insulin and maximal at 10(-6) M. The phosphorylated 92,000 Mr protein band from detergent-solubilized basolateral membranes was immunoprecipitated using serum from a patient with anti-receptor antibodies. No insulin-stimulated phosphorylation was detected in brush border membranes. Binding of insulin to membranes was highly specific for native hormone and was severalfold greater in basolateral membranes than in brush border membranes. These observations are consistent with the asymmetrical distribution of insulin-stimulated protein kinase as well as specific insulin binding sites in the proximal tubular cell. The data suggest that insulin exerts physiological effects on the cell through binding to specific basolateral membrane receptors and phosphorylation of those receptors.
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PMID:Insulin-stimulated phosphorylation and insulin binding in canine renal basolateral membranes. 638 75

With a view to obtaining a more complete view of the composition and structure of the thick filaments of vertebrate skeletal muscle, we have isolated and characterized two new myofibrillar components, H-protein and X-protein. These were purified by hydroxyapatite column chromatography of an impure C-protein preparation itself made from impure myosin extracted from rabbit back and leg muscles. H-protein is the protein responsible for band H on sodium dodecyl sulphate/polyacrylamide gel electrophoresis of crude myosin. X-protein, although present in such preparations in significant quantities, was not detected previously since it is difficult to resolve from C-protein by sodium dodecyl sulphate/polyacrylamide gel electrophoresis. Physical-chemical parameters have been determined for the new proteins and compared with those of C-protein. The apparent chain weight of H-protein estimated by sodium dodecyl sulphate/polyacrylamide gel electrophoresis is 69,000, whereas that of X-protein (152,000) is only slightly greater than that of C-protein (140,000). The molecular weights of H- and X-proteins determined by sedimentation equilibrium centrifugation show that the molecules contain only a single polypeptide chain. The circular dichroism spectra indicate that the proteins have low alpha-helical contents. Both proteins, particularly H-protein, have a high proline content. Although X-protein is of similar chain weight to C-protein, the two show distinct differences in other properties. The sedimentation coefficient of X-protein is markedly lower than that of C-protein, suggesting X-protein is a more asymmetrical molecule. The amino acid compositions, although broadly similar, also show clear differences. Antibodies to H-protein, X-protein and C-protein have been raised in goats and shown not to cross-react.
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PMID:H-protein and X-protein. Two new components of the thick filaments of vertebrate skeletal muscle. 641 90

We have investigated the symmetry of Na+-succinate cotransport in rabbit renal brush-border membrane vesicles. Succinate influx and efflux kinetics were measured under voltage-clamped conditions using [14C]succinate and a rapid filtration procedure. Both influx and efflux were Na+-dependent, saturable, temperature-sensitive, and influenced by the trans Na+ and succinate concentrations. The system was judged to be asymmetric, since the maximal velocity for influx was 3-fold higher than that for efflux, and trans Na+ inhibited influx more than efflux. This may be due to the asymmetrical insertion of the transporter in the brush-border membrane, which leads to differences in either the forward and backward translocation rates of the fully loaded carrier or the Na+ and succinate binding constants at the inner and outer faces of the membrane.
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PMID:Asymmetry of the Na+-succinate cotransporter in rabbit renal brush-border membranes. 646 57

The effect of severe zinc deficiency on the distribution of nine elements (potassium, phosphorus, sodium, magnesium, calcium, iron, zinc, copper and manganese) in brain regions (olfactory lobes, right and left hippocampi, cerebellum and the rest of the brain) has been studied. After male rats (30 days old) were fed a zinc-deficient diet for 28 days, the zinc concentration of most brain parts was similar to zinc-adequate control values. Olfactory lobe zinc, on the other hand, was slightly depressed. However, the levels of other metals were dependent on zinc nutriture. Zinc deficiency caused an elevation in copper concentrations in most brain parts. Restriction of food intake caused a similar increase in brain copper but generally the effect was less than with zinc deficiency. Levels of calcium, manganese, sodium and potassium, in certain brain regions, also appeared to be altered by the zinc status of an animal. Of the minerals examined, only zinc and copper displayed asymmetrical distribution between the right and left hippocampus, and severe zinc deficiency did not affect lateral distribution of these trace metals in the hippocampus. The data suggest the hypothesis that changes in brain metal content, associated with zinc deficiency, contribute to the behavioral abnormalities that occur.
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PMID:Severe zinc deficiency: effects on the distribution of nine elements (potassium, phosphorus, sodium, magnesium, calcium, iron, zinc, copper and manganese) in regions of the rat brain. 661 70

The beta-diketone 1,1,1,2,2,3,3-heptafluoro-7,7-dimethyloctane-4,6-dione (FOD) translocates calcium from an aqueous medium into an organic phase. FOD is less efficient than but acts synergistically with A23187 in causing calcium translocation. The FOD-mediated process of calcium translocation is inhibited by NaCl, although the translocation of sodium by FOD is two to three orders of magnitude lower than that of calcium, when expressed relative to the concentration of these cations in the aqueous medium. At pH 7.4, FOD mediates calcium exchange-diffusion in fluid liposomes as efficiently as A23187. The extent of exchange-diffusion depends on the rigidity and cholesterol content of the liposomes. Conformational analysis of the complex formed by two molecules of FOD and one calcium atom at a simulated membrane interface reveals the existence of several interconvertible, asymmetrical and more-or-less planar configurations. The efficiency of FOD-mediated calcium ionophoresis thus appears to be regulated in a multifactorial manner by such factors as the concentration of calcium and monovalent cations, chemical composition and fluidity of the membrane, availability of other ionophoretic molecules and spatial configuration of the calcium complex.
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PMID:Calcium transport by a beta-diketone in model membranes. 662 22

We studied the uptake of leucine, phenylalanine, and the amino acid analog, 2-aminonorborane-2-carboxylic acid, by rat hepatoma cells in tissue culture. The uptake of these amino acids was partially mediated by a plasma membrane transport system similar to the L agency described in other cell types in that it does not require extracellular sodium and is subject to trans-stimulation. Initial rates of sodium-independent transport of these amino acids were calculated using mathematical transformations of the uptake time course curves. The glucocorticoid dexamethasone inhibits the activity of this transport system; the initial rates of sodium-independent uptake of leucine, phenylalanine, and 2-aminonorborane-2-carboxylic acid are decreased by approximately one-third (average = 30%, n = 19) after incubation of HTC cells with 0.1 microM dexamethasone. This inhibition requires at least 15 h, reaching a maximum at 24 h of exposure of the cells to the hormone. Dexamethasone has an asymmetrical effect on sodium-independent amino acid transport in that exposure of the cells to the hormone does not inhibit the rates of outflow of leucine or phenylalanine from preloaded cells into medium without sodium. Inhibition of uptake is blocked by 0.1 mM cycloheximide and 4 microM actinomycin D, indicating the need for continuous protein synthesis for dexamethasone action. Insulin, which is known to partially reverse the inhibitory effect of dexamethasone on the A amino acid transport system in HTC cells, does not alter the action of dexamethasone on the L system. Previous investigations have demonstrated inhibition by dexamethasone of at least two distinct sodium-dependent amino acid transport activities in HTC cells. The data presented here, showing inhibition by the glucocorticoid of a sodium-independent transport activity, indicate that the effect of the hormone is independent of the energy source of the amino acid transport systems affected.
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PMID:Inhibition of sodium-independent amino acid transport by dexamethasone in rat hepatoma cells. 670 44

Twelve healthy male volunteers participated in a balanced crossover comparison of a brand-name and generic furosemide formulations. Each treatment was given as a single 40-mg tablet following an overnight fast. Furosemide concentrations in plasma and urine were determined up to 24 h after treatment; urine output and urinary sodium excretion were also measured. In comparison with the brand-name tablets, generic furosemide was significantly less bioavailable. Using a 95% confidence interval approach, generic furosemide gave up to 66% lower maximum furosemide plasma levels, up to 52% less area under the plasma level curve to infinite time, and up to 37% less urinary recovery of furosemide. Comparison of the effect of the two treatments was a less sensitive measurement of bioequivalence. Confidence intervals for differences in urinary output and sodium excretion over the period of maximum effect (0-4 h) were, however, asymmetrical, and pharmacodynamic differences between treatments were significant at the 10% level.
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PMID:Comparative bioavailability of two furosemide formulations in humans. 672 24

RX 336-M (7,8-dihydro-5',6'-dimethylcyclohex-5'-eno-1',2',8',14 codeinone) and four other chemically-diverse agents--AG-3-5 (1-[2-hydroxyphenyl]-4-[3-nitrophenyl]-1,2,3,6-tetrahydropyrimidine-2-one), Sgd 8473 (alpha-[4-chlorobenzylideneamino)-oxy]-isobutyric acid), thyrotropin releasing hormone (TRH), and sodium valproate--each induce signs of withdrawal, most notably 'wet-dog' shaking, after acute i.p. administration in drug-naive rats. They are therefore additions to a recently recognized and, as yet, ill-defined class of behaviorally active compounds. The pharmacological baselines that link these disparate agents together have been studied in the present work, using 'wet-dog' shaking as the behavioral measure and RX 336-M as the reference shake-inducing compound. Peripheral administration of clonidine, haloperidol, d-lysergic acid diethylamide, or morphine suppressed chemically induced shaking: naloxone had no marked effect. Reverse tolerance was associated with TRH-induced shaking whereas tolerance occurred with the other four compounds. Cross-tolerance interactions were asymmetrical. Thus, rats rendered tolerant to RX 336-M were cross-tolerant to AG-3-5, TRH, and sodium valproate but not to Sgd 8473; in contrast, RX 336-M-induced shaking was only significantly reduced in rats made tolerant to Sgd 8473. In view of the unidirectional nature of the cross-tolerance relationships studied, it is concluded that AG-3-5, Sgd 8473, sodium valproate, and TRH initiate 'wet-dog' shaking through neural substrates that differ from the one(s) associated with RX 336-M. Nevertheless, all five compounds may eventually trigger a common shake-inducing mechanism.
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PMID:RX 336-M, a new chemical tool in the analysis of the quasi-morphine withdrawal syndrome. 678 43

The bidirectional fluxes and energetics of methotrexate transport in Ehrlich ascites tumor cells were profoundly altered in a high [K+], low [Na+] buffer (K+ buffer). Incubation of cells for 30 min in K+ buffer reduced influx by 27% and the efflux rate constant by 53%. This asymmetrical inhibition of bidirectional fluxes increased the net exchangeable intracellular methotrexate level per cell, but the actual intracellular methotrexate concentration at the steady state was similar to that in Na+ buffer, since the high [K+] caused an increase in intracellular water. Because cells exposed to K+ buffer were depolarized, the apparent electrochemical potential difference for methotrexate was markedly reduced. However, the steady-state intracellular methotrexate level was still related to the extracellular concentration by an absorption isotherm, indicating asymmetry in the bidirectional fluxes similar to that observed in Na+ buffer and thus predicting that transmembrane gradients would be produced at very low extracellular methotrexate concentrations. Glucose, which had little effect on bidirectional fluxes and reduced the steady-state level of methotrexate in Na+ buffer, stimulated influx, inhibited efflux and rapidly increased the steady state in K+ buffer similar to the effects of glucose in the presence of glucose in the presence of iodoacetate in Na+ buffer. Finally, cells exposed to k+ buffer exhibited trans-stimulation of [3H]methotrexate influx when loaded with non-labeled methotrexate, a phenomenon not observed in Na+ buffer. The results indicate that although methotrexate transport is not affected by transient changes in the cationic composition of the extracellular compartment, prolonged exposure of cells to a high [K+], low [Na+] environment markedly alters the physical properties of the cells and the transport parameters for methotrexdate and reveals characteristics of the methotrexate carrier system that are not evident in other buffer systems.
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PMID:K+-induced alterations of energetics and exchange diffusion in the carrier-mediated transport of the folic acid analog, methotrexate, in Ehrlich ascites tumor cells. 719 70

Oxygen tension differences across the mouse ear have been measured polarographically under conditions of no blood flow. For some experiments the ear was split into two by cleavage along the central cartilage plate, and the diffusion of oxygen measured in both directions across these asymmetrical preparations. Measurements were also made on ears from which the stratum corneum had been removed by stripping with Sellotape. It was possible to relate these results to a simple multi-layer diffusion model. The main barrier to diffusion of oxygen resides in the stratum corneum, whose permeability is estimated to be 1 . 2 X 10(-8) ml O2 atm-1 cm-1 S-1. The permeability of the rest of the ear is 4 . 7 X 10(-7) ml O2 atm-1 cm-1 S-1. The inhibition of tissue respiration by the local injection of solutions of sodium amytal, potassium cyanide and other substances reduced the oxygen gradients by factors of between 3 and 7. Cooling the ear from room temperature to 0 degree C reduced the gradients by a factor of about 4.
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PMID:Diffusion of oxygen through the mouse ear. 725 78


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