SUBCELLULAR LOCALIZATION
| plasma membrane
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| intracellular
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| intracellular,cytoplasm,organelle,membrane
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| intracellular,cytoplasm,organelle,Golgi
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| intracellular,cytoplasm,organelle,endosome
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| intracellular,cytoplasm,organelle,lysosome
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| intracellular,cytoplasm,cytosolic
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| text
| expressed in endosomes and apical membranes of renal tubules  |
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| basic FUNCTION
| chloride voltage-gated channel, likely involved in the receptor-mediated endocytic pathway |
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functioning as electrogenic Cl-/H+ exchanger, carrying a substantial amount of protons across the plasma membrane when activated by positive voltages |
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playing a role in the activation of apical protein endocytosis in kidney proximal tubules by regulating trafficking of megalin and cubilin at the brush border |
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electrically shunting Cl- channel in early endosomes, facilitating intraluminal acidification |
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may compensate the charge accumulation by endosomal proton pumps |
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playing a definitive role in the trafficking and acidification-dependent recycling of apical membrane proteins |
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regulates dentin development through TGFB1 pathway |
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interaction with KIF3B is important for CLCN5 plasma membrane expression and for facilitating endocytosis and microtubular transport in the kidney |
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endosomal chloride concentration, which is raised by CLCN5 in exchange for protons accumulated by the H+-ATPase, may play a role in endocytosis |
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essential for the endocytic activity of the proximal tubule cells and the tubular clearance of proteins filtered in the glomeruli |
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role of CFTR and CLCN5 in modulating vacuolar H+-ATPase activity in kidney proximal tubule |
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Cl-/H+ antiporters that carry out fundamental physiological tasks by transporting Cl- across plasma membrane and intracellular compartments |
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in addition to defective endocytosis, proximal tubule cells lacking CLCN5 show a trafficking defect in apical receptors and transporters, as well as lysosomal dysfunction and typical features of dedifferentiation, proliferation and oxidative stress |
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CLCN3 and CLCN5 are necessary components for S1P-induced excitatory Cl- currents but not for the amplification of TRPV1-mediated currents in sensory neurons |
