Membrane chloride transport

Membrane chloride transport (e.g. sodium-dependent transport. Renal brush-border, GABAa receptor),... 

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... 

BE Schaeffer, JA Zadunaisky. (1979). Stimulation of chloride transport by fatty acids in corneal epithelium and relation to changes in membrane fluidity. Biochim Biophys Acta 556 131-143. 

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... 

Cyclodiene pesticides, of which endrin and its oxidized analogs are representative, can also be estimated by receptor-assay technique. Cyclodiene pesticides exert their mode of action by altering central nervous system membrane ion transport. In work reported by Saleh et al. (1993), a labeled amino acid, GABA, that binds to the chloride channel receptor is displaced by endrin (and other similar molecules), and thus serves as an assay for these pesticides. The GABA receptor was shown to be a potentially useful biomarker for organochlorine pesticides such as lindane, toxaphene, endrin, chlordane, and others. The assay involves small quantities of blood (0.1 mL), and requires only that the plasma be separated from the... 

INTESTINE Characterization of a membrane potassium ion conductance in intestinal secretory cells using whole cell patch-clamp and calcium-sensitive dye techniques, 192, 309 isolation of intestinal epithelial cells and evaluation of transport functions, 192, 324 isolation of enterocyte membranes, 192, 341 established intestinal cell lines as model systems for electrolyte transport studies, 192, 354 sodium chloride transport pathways in intestinal membrane vesicles, 192, 389 advantages and limitations of vesicles for the characterization and the kinetic analysis of transport systems, 192, 409 isolation and reconstitution of the sodium-de-pendent glucose transporter, 192, 438 calcium transport by intestinal epithelial cell basolateral membrane, 192, 448 electrical measurements in large intestine (including cecum, colon, rectum), 192, 459... 

Zhao, Z., Li, X., Hao, J., Winston, J. H., and Weinman, S. A. (2007) The ClC-3 chloride transport protein traffics through the plasma membrane via interaction of an N-terminal dileucine cluster with clathrin J Biol Chem 282,29022-29031. 

Ion transport pathways across the luminal and basolateral membranes of the distal convoluted tubule cell. As in all tubular cells, Na+/K+ ATPase is present in the basolateral membrane. NCC is the primary sodium and chloride transporter in the luminal membrane. (R, parathyroid hormone [PTH] receptor.)... 

In summary, there is evidence that the skin presents a weak cation permselectivity [25,76,77,80,93,125], which can be reversed by acidifying the pH of the solutions bathing the skin [10,23,76,77]. At pH>p/, the skin is negatively charged and electroosmotic flow proceeds in the anode-to-cathode direction. At pH < pi, the skin becomes positively charged and electroosmotic flow reverses to the cathode-to-anode direction. Under the application of an electric field, counterions (cations at physiological pH) are preferentially admitted into the skin. As a consequence, the sodium and chloride transport numbers are 0.6 and 0.4, respectively, during transdermal iontophoresis (in contrast to their values in a neutral membrane tNa = 0.45 rCi = 0.55) [126]. 

Chronic diseases include cystic fibrosis in which nasal mucus is thick and viscous as a result of abnormal chloride transport across the membrane of the epithelial cells, leading to reduced water secretion. Similarly, chronic sinusitis also reduces nasal mucociliary clearance due to an increase in the rheological properties of mucus. 

Figure 2. Bulk calcium transport by the osteoclast. Net acid transport is driven by the vacuolar-type H+-ATPase with a specialized large membrane subunit. Transport is balanced by chloride transport, probably involving both a chloride channel (CLIC-5) and a chloride bicarbonate antiporter (CLCN7). Supporting transport processes include chloride-bicarbonate exchange. Insertion of transporters is specific for subcellular locations and involves interaction of transporters with specific cytoskeletal components, including actin (See Colour Plate 29)...

Figure 4.40 Chloride transport by a lipid vesicle membrane-incorporated cholapod. Chloride flux from outside to inside the vesicle quenches the fluorescence of the lucigenin dye in the interior of the system.

Genetic alterations or abnormalities of germ cells, some of which can be caused by toxicant exposure, can be manifested by adverse effects on progeny. The important health effects of these kinds of alterations may be appreciated by considering the kinds of human maladies that are caused by inherited recessive mutations. One such disease is cystic fibrosis, in which the clinical phenotype has thick, dry mucus in the tubes of the respiratory system such that inhaled bacterial and fungal spores cannot be cleared from the system. This results in frequent, severe infections. It is the consequence of a faulty chloride transporter membrane protein that does not properly transport Cl ion from inside cells to the outside, where they normally retain water characteristic of healthy mucus. The faulty transporter protein is the result of a change of a single amino acid in the protein. 

Gerenscser, G. Ed. Chloride Transport Coupling in Biological Membranes and Epithelia, Elsevier Amsterdam, 1984. 

It has recently been suggested that stimulation of gastric acid secretion across the apical membrane of the gastric parietal cell predominantly reflects the insertion of an active potassium and chloride transporter/ channel rather than direct activation of HVK -ATPase. However, the mechanisms involved in and Cl transport into the gastric parietal cell are still controversial. The presence of a Cl channel in the apical membrane has been confirmed by using established d channel blockers. In vitro in rabbit isolated gastric parietal cells, 9-anthracene carboxylate and the more potent diphenylamine-2-carboxylate inhibit gastric acid formation concen-tration-dependently irrespective of the kind of stimulation [181]. Thus Cl channel blockers can be defined as indirect HVK -ATPase inhibitors. 

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