Plasma membrane proton transport

Oxidase Control of Plasma Membrane Proton Transport... 

Transport proteins (channels) for chloride and zinc Vacuolar proton pump Components of synaptic vesicles to mediate the chloride flux for glutamate uptake and zinc uptake in most synaptic vesicles. Zinc transporter is homologous to endosomal and plasma membrane zinc transporters chloride transporters remain to be identified. Protein complex of more than 12 subunits. Constitutes the largest component of synaptic vesicles and establishes... 

Her research interests originally focused on biological cell membranes, first working on phosphate transport in Escherichia coli and then the plasma membrane proton ATPase in Saccharomyces cerevisiae. While isolating vanadate-resistant mutants in yeast, she became fascinated with work showing that oral administration of vanadium salts alleviated symptoms of diabetes and switched her research focus to that area. She has pursued the insulin-enhancing mechanism of vanadium salts and complexes in cell culture, the STZ-induced diabetic rat, and human type 2 diabetic patients. The National Institutes of Health, the American Heart Association, and the American Diabetes Association have funded the work in her laboratory. Willsky has lectured all around the world and published both research articles and book chapters in this area. 

In this chapter the evidence for activation of some of these known channels by plasma membrane electron transport or the direct action of the oxidoreductase in proton movement is discussed. 

Although plasma membrane monoamine transporters are responsible for the reuptake of neurotransmitters from the synapse, vesicular monoamine transporters (VMAT) sequester monoamines into synaptic vesicles in preparation for fusion with the plasma membrane and release into the synapse (Schuldiner et ah, 1995). Vesicular uptake is coupled to a proton gradient across the vesicle membrane rather than the sodium gradient used with the plasma membrane transporters (Schuldiner et ah, 1995). These vesicular transporters are not neurotransmitter-speciflc rather, they transport the monoamines nonselectively (Johnson, Jr., 1988 Henry et ah, 1998). 

Zhou, M., Xia, L. and Wang, J. (2007) Metformin transport by a newly cloned proton-stimulated organic cation transporter (plasma membrane monoamine transporter) expressed in human intestine. Drug Metabolism and Disposition The Biological Fate of Chemicals, 35 (10), 1956—1962. 

Fig. 3 A, B. The two mechanisms of xylose uptake by yeast A facilitated diffusion - the driving force is the concentration gradient between the medium and the cytosol - these transporters generally have a broad substrate range B proton-xylose symport. - the driving force is the proton motive force, which is maintained by the plasma membrane proton-ATPase. Adapted from [109]...

C.L. Slayman, Charge-transport characteristics of a plasma membrane proton pump in Membranes and Transport, vol. 1 (Plenum Press, New York, 1982) pp. 485 90... 

C1C-6 is a late endosomal chloride transporter. Its disruption in mice led to lysosomal storage disease. C1C-7 is expressed in late endosomes and lysosomes. It needs Ostml as (3-subunit [3]. The disruption of either C1C-7 or Ostml in mice and man leads to severe osteopetrosis, retinal degeneration, and a severe lysosomal storage disease. ClC-7/Ostml is highly expressed in osteoclasts. In these cells, it is inserted together with the proton pump into the specialized plasma membrane ( ruffled border ) that faces the reabsorption lacuna. Osteoclasts are still present in C1C-7 knockout... 

Synaptic vesicles isolated from brain exhibit four distinct vesicular neurotransmitter transport activities one for monoamines, a second for acetylcholine, a third for the inhibitory neurotransmitters GABA and glycine, and a fourth for glutamate [1], Unlike Na+-dependent plasma membrane transporters, the vesicular activities couple to a proton electrochemical gradient (A. lh+) across the vesicle membrane generated by the vacuolar H+-ATPase ( vacuolar type proton translocating ATPase). Although all of the vesicular transport systems rely on ApH+, the relative dependence on the chemical and electrical components varies (Fig. 1). The... 

Figure 7 Mixld for iron (Fe) deficiency induced changes in root physiology and rhizo-sphere chemistry associated with Fc acquisition in strategy I plants. (Modified froin Ref. 1.) A. Stimulation of proton extru.sion by enhanced activity of the plasnialemma ATPase —> Felll solubilization in the rhizospherc. B. Enhanced exudation of reductanls and chela-tors (carhoxylates. phenolics) mediated by diffusion or anion channels Pe solubilization by Fein complexation and Felll reduction. C. Enhanced activity of plasma membrane (PM)-bound Felll reductase further stimulated by rhizosphere acidificalion (A). Reduction of FolII chelates, liberation of Fell. D. Uptake of Fell by a PM-bound Fell transporter.

As we saw in the previous section, Strategy 1 plants utilize ferric reductases, with NADPH as electron donor, coupled to proton extrusion and a specific Fe(II) transport system localized in the root plasma membrane. Saccharomyces cerevisiae also uses cell surface reductases to reduce ferric iron, and in early studies (Lesuisse et ah, 1987 ... 

Monocarboxylates such as lactic acid and pyruvate are transported across plasma membranes by members of the proton-linked monocarboxylate transporter (MCT)... 

The intestinal absorption of dietary cholesterol esters occurs only after hydrolysis by sterol esterase steryl-ester acylhydrolase (cholesterol esterase, EC 3.1.1.13) in the presence of taurocholate [113][114], This enzyme is synthesized and secreted by the pancreas. The free cholesterol so produced then diffuses through the lumen to the plasma membrane of the intestinal epithelial cells, where it is re-esterified. The resulting cholesterol esters are then transported into the intestinal lymph [115]. The mechanism of cholesterol reesterification remained unclear until it was shown that cholesterol esterase EC 3.1.1.13 has both bile-salt-independent and bile-salt-dependent cholesterol ester synthetic activities, and that it may catalyze the net synthesis of cholesterol esters under physiological conditions [116-118], It seems that cholesterol esterase can switch between hydrolytic and synthetic activities, controlled by the bile salt and/or proton concentration in the enzyme s microenvironment. Cholesterol esterase is also found in other tissues, e.g., in the liver and testis [119][120], The enzyme is able to catalyze the hydrolysis of acylglycerols and phospholipids at the micellar interface, but also to act as a cholesterol transfer protein in phospholipid vesicles independently of esterase activity [121],... 

An important point to note is that this the above reaction produces lactate, not lactic acid. Nonetheless, protons are produced in glycolysis but in another reaction (Appendix 6.5). Consequently, the two end-products are lactate plus protons, which can be described as lactic acid. Despite this discussion, it can be argued that lactate dehydrogenase is not the terminal reaction of glycolysis, since the lactate plus protons have to be transported out of the cell into the interstitial space. This requires a transporter protein, which transports both lactate and protons across the plasma membrane and out of the cell. 

Aminoglycosides must traverse the plasma membrane and, in the case of gramnegative bacteria, the outer membrane to gain access to the target ribosomes. Transport across the plasma membrane has been shown to require the proton motive force, and mutants deficient in electron transport chain components fail to transport aminoglycosides and are consequently resistant. ... 

Boron also appears to be involved in redox metabolism in cell membranes. Boron deficiency was shown to inhibit membrane H -ATPase isolated from plant roots, and H -ATPase-associated proton secretion is decreased in boron-deficient cell cultures [71]. Other studies show an effect of boron on membrane electron transport reactions and the stimulation of plasma reduced nicotinamide adenine dinucleotide (NADH) oxidase upon addition of boron to cell cultures [72, 73]. NADH oxidase in plasma membrane is believed to play a role in the reduction of ascorbate free radical to ascorbate [74]. One theory proposes that, by stimulating NADH oxidase to keep ascorbate reduced at the cell wall-membrane interface, the presence of boron is important in... 

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