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New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development
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Zeitschriftentitel: | Kidney Diseases |
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Personen und Körperschaften: | , |
In: | Kidney Diseases, 2, 2016, 3, S. 128-135 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
S. Karger AG
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Schlagwörter: |
author_facet |
Wu, Ming Yu, Shengqiang Wu, Ming Yu, Shengqiang |
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author |
Wu, Ming Yu, Shengqiang |
spellingShingle |
Wu, Ming Yu, Shengqiang Kidney Diseases New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development Marketing Organizational Behavior and Human Resource Management Strategy and Management Drug Discovery Pharmaceutical Science Pharmacology |
author_sort |
wu, ming |
spelling |
Wu, Ming Yu, Shengqiang 2296-9381 2296-9357 S. Karger AG Marketing Organizational Behavior and Human Resource Management Strategy and Management Drug Discovery Pharmaceutical Science Pharmacology http://dx.doi.org/10.1159/000444839 <jats:p><b><i>Background:</i></b> Autosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the <i>PKD1</i>, <i>PKD2</i> or <i>PKHD1 </i>gene, which encodes polycystin-1, polycystin-2 or fibrocystin, respectively. Embryonic and postnatal mutation studies show that transport or channel function is dysregulated before the initiation of cystogenesis, suggesting that the abnormality of transport or channel function plays a critical role in the pathology of PKD. <b><i>Summary:</i></b> Polycystin-2 by itself is a calcium-permeable cation channel, and its channel function can be regulated by polycystin-1 or fibrocystin. In this paper, we reviewed the current knowledge about calcium transports and cyclic adenosine monophosphate (cAMP)-driven chloride transports in PKD. In addition, the function and the underlining mechanism of glucose transporters, phosphate transporters and water channels in PKD are also discussed. <b><i>Key Messages:</i></b> Abnormalities in calcium handling and exuberant cAMP-dependent cystic fibrosis transmembrane conductance regulator-mediated fluid secretion in the collecting duct are the most important issues in the pathogenesis of PKD.</jats:p> New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development Kidney Diseases |
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10.1159/000444839 |
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Wirtschaftswissenschaften Chemie und Pharmazie |
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Kidney Diseases |
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title |
New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_unstemmed |
New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_full |
New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_fullStr |
New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_full_unstemmed |
New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_short |
New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_sort |
new insights into the molecular mechanisms targeting tubular channels/transporters in pkd development |
topic |
Marketing Organizational Behavior and Human Resource Management Strategy and Management Drug Discovery Pharmaceutical Science Pharmacology |
url |
http://dx.doi.org/10.1159/000444839 |
publishDate |
2016 |
physical |
128-135 |
description |
<jats:p><b><i>Background:</i></b> Autosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the <i>PKD1</i>, <i>PKD2</i> or <i>PKHD1 </i>gene, which encodes polycystin-1, polycystin-2 or fibrocystin, respectively. Embryonic and postnatal mutation studies show that transport or channel function is dysregulated before the initiation of cystogenesis, suggesting that the abnormality of transport or channel function plays a critical role in the pathology of PKD. <b><i>Summary:</i></b> Polycystin-2 by itself is a calcium-permeable cation channel, and its channel function can be regulated by polycystin-1 or fibrocystin. In this paper, we reviewed the current knowledge about calcium transports and cyclic adenosine monophosphate (cAMP)-driven chloride transports in PKD. In addition, the function and the underlining mechanism of glucose transporters, phosphate transporters and water channels in PKD are also discussed. <b><i>Key Messages:</i></b> Abnormalities in calcium handling and exuberant cAMP-dependent cystic fibrosis transmembrane conductance regulator-mediated fluid secretion in the collecting duct are the most important issues in the pathogenesis of PKD.</jats:p> |
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author | Wu, Ming, Yu, Shengqiang |
author_facet | Wu, Ming, Yu, Shengqiang, Wu, Ming, Yu, Shengqiang |
author_sort | wu, ming |
container_issue | 3 |
container_start_page | 128 |
container_title | Kidney Diseases |
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description | <jats:p><b><i>Background:</i></b> Autosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the <i>PKD1</i>, <i>PKD2</i> or <i>PKHD1 </i>gene, which encodes polycystin-1, polycystin-2 or fibrocystin, respectively. Embryonic and postnatal mutation studies show that transport or channel function is dysregulated before the initiation of cystogenesis, suggesting that the abnormality of transport or channel function plays a critical role in the pathology of PKD. <b><i>Summary:</i></b> Polycystin-2 by itself is a calcium-permeable cation channel, and its channel function can be regulated by polycystin-1 or fibrocystin. In this paper, we reviewed the current knowledge about calcium transports and cyclic adenosine monophosphate (cAMP)-driven chloride transports in PKD. In addition, the function and the underlining mechanism of glucose transporters, phosphate transporters and water channels in PKD are also discussed. <b><i>Key Messages:</i></b> Abnormalities in calcium handling and exuberant cAMP-dependent cystic fibrosis transmembrane conductance regulator-mediated fluid secretion in the collecting duct are the most important issues in the pathogenesis of PKD.</jats:p> |
doi_str_mv | 10.1159/000444839 |
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spelling | Wu, Ming Yu, Shengqiang 2296-9381 2296-9357 S. Karger AG Marketing Organizational Behavior and Human Resource Management Strategy and Management Drug Discovery Pharmaceutical Science Pharmacology http://dx.doi.org/10.1159/000444839 <jats:p><b><i>Background:</i></b> Autosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the <i>PKD1</i>, <i>PKD2</i> or <i>PKHD1 </i>gene, which encodes polycystin-1, polycystin-2 or fibrocystin, respectively. Embryonic and postnatal mutation studies show that transport or channel function is dysregulated before the initiation of cystogenesis, suggesting that the abnormality of transport or channel function plays a critical role in the pathology of PKD. <b><i>Summary:</i></b> Polycystin-2 by itself is a calcium-permeable cation channel, and its channel function can be regulated by polycystin-1 or fibrocystin. In this paper, we reviewed the current knowledge about calcium transports and cyclic adenosine monophosphate (cAMP)-driven chloride transports in PKD. In addition, the function and the underlining mechanism of glucose transporters, phosphate transporters and water channels in PKD are also discussed. <b><i>Key Messages:</i></b> Abnormalities in calcium handling and exuberant cAMP-dependent cystic fibrosis transmembrane conductance regulator-mediated fluid secretion in the collecting duct are the most important issues in the pathogenesis of PKD.</jats:p> New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development Kidney Diseases |
spellingShingle | Wu, Ming, Yu, Shengqiang, Kidney Diseases, New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development, Marketing, Organizational Behavior and Human Resource Management, Strategy and Management, Drug Discovery, Pharmaceutical Science, Pharmacology |
title | New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_full | New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_fullStr | New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_full_unstemmed | New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_short | New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
title_sort | new insights into the molecular mechanisms targeting tubular channels/transporters in pkd development |
title_unstemmed | New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development |
topic | Marketing, Organizational Behavior and Human Resource Management, Strategy and Management, Drug Discovery, Pharmaceutical Science, Pharmacology |
url | http://dx.doi.org/10.1159/000444839 |