author_facet Wu, Ming
Yu, Shengqiang
Wu, Ming
Yu, Shengqiang
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>&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; Autosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the &lt;i&gt;PKD1&lt;/i&gt;, &lt;i&gt;PKD2&lt;/i&gt; or &lt;i&gt;PKHD1 &lt;/i&gt;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. &lt;b&gt;&lt;i&gt;Summary:&lt;/i&gt;&lt;/b&gt; 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. &lt;b&gt;&lt;i&gt;Key Messages:&lt;/i&gt;&lt;/b&gt; 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
doi_str_mv 10.1159/000444839
facet_avail Online
Free
finc_class_facet Wirtschaftswissenschaften
Chemie und Pharmazie
format ElectronicArticle
fullrecord blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OS8wMDA0NDQ4Mzk
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OS8wMDA0NDQ4Mzk
institution DE-Zi4
DE-Gla1
DE-15
DE-Pl11
DE-Rs1
DE-14
DE-105
DE-Ch1
DE-L229
DE-D275
DE-Bn3
DE-Brt1
DE-Zwi2
DE-D161
imprint S. Karger AG, 2016
imprint_str_mv S. Karger AG, 2016
issn 2296-9357
2296-9381
issn_str_mv 2296-9357
2296-9381
language English
mega_collection S. Karger AG (CrossRef)
match_str wu2016newinsightsintothemolecularmechanismstargetingtubularchannelstransportersinpkddevelopment
publishDateSort 2016
publisher S. Karger AG
recordtype ai
record_format ai
series Kidney Diseases
source_id 49
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>&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; Autosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the &lt;i&gt;PKD1&lt;/i&gt;, &lt;i&gt;PKD2&lt;/i&gt; or &lt;i&gt;PKHD1 &lt;/i&gt;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. &lt;b&gt;&lt;i&gt;Summary:&lt;/i&gt;&lt;/b&gt; 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. &lt;b&gt;&lt;i&gt;Key Messages:&lt;/i&gt;&lt;/b&gt; 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>
container_issue 3
container_start_page 128
container_title Kidney Diseases
container_volume 2
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
_version_ 1792333469017178128
geogr_code not assigned
last_indexed 2024-03-01T14:13:14.782Z
geogr_code_person not assigned
openURL url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=New+Insights+into+the+Molecular+Mechanisms+Targeting+Tubular+Channels%2FTransporters+in+PKD+Development&rft.date=2016-01-01&genre=article&issn=2296-9357&volume=2&issue=3&spage=128&epage=135&pages=128-135&jtitle=Kidney+Diseases&atitle=New+Insights+into+the+Molecular+Mechanisms+Targeting+Tubular+Channels%2FTransporters+in+PKD+Development&aulast=Yu&aufirst=Shengqiang&rft_id=info%3Adoi%2F10.1159%2F000444839&rft.language%5B0%5D=eng
SOLR
_version_ 1792333469017178128
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
container_volume 2
description <jats:p>&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; Autosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the &lt;i&gt;PKD1&lt;/i&gt;, &lt;i&gt;PKD2&lt;/i&gt; or &lt;i&gt;PKHD1 &lt;/i&gt;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. &lt;b&gt;&lt;i&gt;Summary:&lt;/i&gt;&lt;/b&gt; 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. &lt;b&gt;&lt;i&gt;Key Messages:&lt;/i&gt;&lt;/b&gt; 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
facet_avail Online, Free
finc_class_facet Wirtschaftswissenschaften, Chemie und Pharmazie
format ElectronicArticle
format_de105 Article, E-Article
format_de14 Article, E-Article
format_de15 Article, E-Article
format_de520 Article, E-Article
format_de540 Article, E-Article
format_dech1 Article, E-Article
format_ded117 Article, E-Article
format_degla1 E-Article
format_del152 Buch
format_del189 Article, E-Article
format_dezi4 Article
format_dezwi2 Article, E-Article
format_finc Article, E-Article
format_nrw Article, E-Article
geogr_code not assigned
geogr_code_person not assigned
id ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OS8wMDA0NDQ4Mzk
imprint S. Karger AG, 2016
imprint_str_mv S. Karger AG, 2016
institution DE-Zi4, DE-Gla1, DE-15, DE-Pl11, DE-Rs1, DE-14, DE-105, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161
issn 2296-9357, 2296-9381
issn_str_mv 2296-9357, 2296-9381
language English
last_indexed 2024-03-01T14:13:14.782Z
match_str wu2016newinsightsintothemolecularmechanismstargetingtubularchannelstransportersinpkddevelopment
mega_collection S. Karger AG (CrossRef)
physical 128-135
publishDate 2016
publishDateSort 2016
publisher S. Karger AG
record_format ai
recordtype ai
series Kidney Diseases
source_id 49
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>&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; Autosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the &lt;i&gt;PKD1&lt;/i&gt;, &lt;i&gt;PKD2&lt;/i&gt; or &lt;i&gt;PKHD1 &lt;/i&gt;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. &lt;b&gt;&lt;i&gt;Summary:&lt;/i&gt;&lt;/b&gt; 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. &lt;b&gt;&lt;i&gt;Key Messages:&lt;/i&gt;&lt;/b&gt; 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