Analysis of opossum kidney NaPi-IIc sodium-dependent phosphate transporter to understand Pi handling in human kidney
Background The role of Na + -dependent inorganic phosphate (Pi) transporters in the human kidney is not fully clarified. Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is caused by loss-of-function mutations in the IIc Na + -dependent Pi transporter (NPT2c/Npt2c/NaPi-IIc) gene. Anoth...
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| Veröffentlicht in: | Clinical and experimental nephrology 2019-03, Vol.23 (3), p.313-324 |
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| creator | Fujii, Toru Shiozaki, Yuji Segawa, Hiroko Nishiguchi, Shiori Hanazaki, Ai Noguchi, Miwa Kirino, Ruri Sasaki, Sumire Tanifuji, Kazuya Koike, Megumi Yokoyama, Mizuki Arima, Yuki Kaneko, Ichiro Tatsumi, Sawako Ito, Mikiko Miyamoto, Ken-ichi |
| description | Background
The role of Na
+
-dependent inorganic phosphate (Pi) transporters in the human kidney is not fully clarified. Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is caused by loss-of-function mutations in the IIc Na
+
-dependent Pi transporter (NPT2c/Npt2c/NaPi-IIc) gene. Another Na
+
-dependent type II transporter, (NPT2A/Npt2a/NaPi-IIa), is also important for renal Pi reabsorption in humans. In mice, Npt2c deletion does not lead to hypophosphatemia and rickets because Npt2a compensates for the impaired Pi reabsorption. To clarify the differences between mouse and human, we investigated the relation between NaPi-IIa and NaPi-IIc functions in opossum kidney (OK) cells.
Methods
We cloned NaPi-IIc from OK cells and created opossum NaPi-IIc (oNaPi-IIc) antibodies. We used oNaPi-IIc small interference (si)RNA and investigated the role of NaPi-IIc in Pi transport in OK cells.
Results
We cloned opossum kidney NaPi-IIc cDNAs encoding 622 amino acid proteins (variant1) and examined their pH- and sodium-dependency. The antibodies reacted specifically with 75-kDa and 150-kDa protein bands, and the siRNA of NaPi-IIc markedly suppressed endogenous oNaPi-IIc in OK cells. Treatment with siRNA significantly suppressed the expression of NaPi-4 (NaPi-IIa) protein and mRNA. oNaPi-IIc siRNA also suppressed Na
+
/H
+
exchanger regulatory factor 1 expression in OK cells.
Conclusion
These findings suggest that NaPi-IIc is important for the expression of NaPi-IIa (NaPi-4) protein in OK cells. Suppression of Npt2c may downregulate Npt2a function in HHRH patients. |
| doi_str_mv | 10.1007/s10157-018-1653-4 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_2120206174</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2120206174</sourcerecordid><originalsourceid>FETCH-LOGICAL-p212t-99fde6f92e7fb031a1625d9a5389270be5181eef9cb61bd88c22e2757b5de3863</originalsourceid><addsrcrecordid>eNpdkU9P3DAQxa0KVOi2H6CXyhKXXgz-E8fxESFKV0ItB3q2nPWENU3sYDuH_fZ4tYuQOL2R5qc3o_cQ-s7oJaNUXWVGmVSEso6wVgrSfELnrBGKKKX1SZ1FwwlTkp2hLzk_U0o7LfVndCaoYKpp1Dkq18GOu-wzjgOOc8x5mfB_7wLs8B_74Ml6vcE5Or9MxMEMwUEoeN7GPG9tAVySDXmOqUDCJeKl7lMuNjj84PG26ujDE_YBb5fJhqPzV3Q62DHDt6Ou0L9ft483v8n937v1zfU9mTnjhWg9OGgHzUENff3YspZLp60UneaK9iBZxwAGvelb1ruu23AOXEnVSweia8UK_Tz4zim-LJCLmXzewDjaAHHJpl6hnLY1iopefECf45JqNnuKadpQVUNboR9HaukncGZOfrJpZ97yrAA_ALmuwhOkdxtGzb40cyjN1NLMvjTTiFcCvYgT</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2119040730</pqid></control><display><type>article</type><title>Analysis of opossum kidney NaPi-IIc sodium-dependent phosphate transporter to understand Pi handling in human kidney</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Fujii, Toru ; Shiozaki, Yuji ; Segawa, Hiroko ; Nishiguchi, Shiori ; Hanazaki, Ai ; Noguchi, Miwa ; Kirino, Ruri ; Sasaki, Sumire ; Tanifuji, Kazuya ; Koike, Megumi ; Yokoyama, Mizuki ; Arima, Yuki ; Kaneko, Ichiro ; Tatsumi, Sawako ; Ito, Mikiko ; Miyamoto, Ken-ichi</creator><creatorcontrib>Fujii, Toru ; Shiozaki, Yuji ; Segawa, Hiroko ; Nishiguchi, Shiori ; Hanazaki, Ai ; Noguchi, Miwa ; Kirino, Ruri ; Sasaki, Sumire ; Tanifuji, Kazuya ; Koike, Megumi ; Yokoyama, Mizuki ; Arima, Yuki ; Kaneko, Ichiro ; Tatsumi, Sawako ; Ito, Mikiko ; Miyamoto, Ken-ichi</creatorcontrib><description>Background
The role of Na
+
-dependent inorganic phosphate (Pi) transporters in the human kidney is not fully clarified. Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is caused by loss-of-function mutations in the IIc Na
+
-dependent Pi transporter (NPT2c/Npt2c/NaPi-IIc) gene. Another Na
+
-dependent type II transporter, (NPT2A/Npt2a/NaPi-IIa), is also important for renal Pi reabsorption in humans. In mice, Npt2c deletion does not lead to hypophosphatemia and rickets because Npt2a compensates for the impaired Pi reabsorption. To clarify the differences between mouse and human, we investigated the relation between NaPi-IIa and NaPi-IIc functions in opossum kidney (OK) cells.
Methods
We cloned NaPi-IIc from OK cells and created opossum NaPi-IIc (oNaPi-IIc) antibodies. We used oNaPi-IIc small interference (si)RNA and investigated the role of NaPi-IIc in Pi transport in OK cells.
Results
We cloned opossum kidney NaPi-IIc cDNAs encoding 622 amino acid proteins (variant1) and examined their pH- and sodium-dependency. The antibodies reacted specifically with 75-kDa and 150-kDa protein bands, and the siRNA of NaPi-IIc markedly suppressed endogenous oNaPi-IIc in OK cells. Treatment with siRNA significantly suppressed the expression of NaPi-4 (NaPi-IIa) protein and mRNA. oNaPi-IIc siRNA also suppressed Na
+
/H
+
exchanger regulatory factor 1 expression in OK cells.
Conclusion
These findings suggest that NaPi-IIc is important for the expression of NaPi-IIa (NaPi-4) protein in OK cells. Suppression of Npt2c may downregulate Npt2a function in HHRH patients.</description><identifier>ISSN: 1342-1751</identifier><identifier>EISSN: 1437-7799</identifier><identifier>DOI: 10.1007/s10157-018-1653-4</identifier><identifier>PMID: 30317447</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Animals ; Antibodies ; Cells, Cultured ; Clonal deletion ; Cloning ; Familial Hypophosphatemic Rickets - etiology ; Humans ; Hypercalciuria ; Hypercalciuria - etiology ; Hypophosphatemia ; Kidney - metabolism ; Kidneys ; Medicine ; Medicine & Public Health ; Mice ; mRNA ; Na+/H+-exchanging ATPase ; Nephrology ; Opossums ; Original Article ; Phosphate Transport Proteins - physiology ; Phosphate transporter ; Phosphates - metabolism ; Proteins ; Reabsorption ; Rickets ; RNA, Small Interfering - genetics ; RNA-mediated interference ; siRNA ; Sodium ; Sodium-Phosphate Cotransporter Proteins, Type IIc - physiology ; Urology ; Xenopus laevis</subject><ispartof>Clinical and experimental nephrology, 2019-03, Vol.23 (3), p.313-324</ispartof><rights>Japanese Society of Nephrology 2018</rights><rights>Clinical and Experimental Nephrology is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-p212t-99fde6f92e7fb031a1625d9a5389270be5181eef9cb61bd88c22e2757b5de3863</cites><orcidid>0000-0002-0905-246X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10157-018-1653-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10157-018-1653-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30317447$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fujii, Toru</creatorcontrib><creatorcontrib>Shiozaki, Yuji</creatorcontrib><creatorcontrib>Segawa, Hiroko</creatorcontrib><creatorcontrib>Nishiguchi, Shiori</creatorcontrib><creatorcontrib>Hanazaki, Ai</creatorcontrib><creatorcontrib>Noguchi, Miwa</creatorcontrib><creatorcontrib>Kirino, Ruri</creatorcontrib><creatorcontrib>Sasaki, Sumire</creatorcontrib><creatorcontrib>Tanifuji, Kazuya</creatorcontrib><creatorcontrib>Koike, Megumi</creatorcontrib><creatorcontrib>Yokoyama, Mizuki</creatorcontrib><creatorcontrib>Arima, Yuki</creatorcontrib><creatorcontrib>Kaneko, Ichiro</creatorcontrib><creatorcontrib>Tatsumi, Sawako</creatorcontrib><creatorcontrib>Ito, Mikiko</creatorcontrib><creatorcontrib>Miyamoto, Ken-ichi</creatorcontrib><title>Analysis of opossum kidney NaPi-IIc sodium-dependent phosphate transporter to understand Pi handling in human kidney</title><title>Clinical and experimental nephrology</title><addtitle>Clin Exp Nephrol</addtitle><addtitle>Clin Exp Nephrol</addtitle><description>Background
The role of Na
+
-dependent inorganic phosphate (Pi) transporters in the human kidney is not fully clarified. Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is caused by loss-of-function mutations in the IIc Na
+
-dependent Pi transporter (NPT2c/Npt2c/NaPi-IIc) gene. Another Na
+
-dependent type II transporter, (NPT2A/Npt2a/NaPi-IIa), is also important for renal Pi reabsorption in humans. In mice, Npt2c deletion does not lead to hypophosphatemia and rickets because Npt2a compensates for the impaired Pi reabsorption. To clarify the differences between mouse and human, we investigated the relation between NaPi-IIa and NaPi-IIc functions in opossum kidney (OK) cells.
Methods
We cloned NaPi-IIc from OK cells and created opossum NaPi-IIc (oNaPi-IIc) antibodies. We used oNaPi-IIc small interference (si)RNA and investigated the role of NaPi-IIc in Pi transport in OK cells.
Results
We cloned opossum kidney NaPi-IIc cDNAs encoding 622 amino acid proteins (variant1) and examined their pH- and sodium-dependency. The antibodies reacted specifically with 75-kDa and 150-kDa protein bands, and the siRNA of NaPi-IIc markedly suppressed endogenous oNaPi-IIc in OK cells. Treatment with siRNA significantly suppressed the expression of NaPi-4 (NaPi-IIa) protein and mRNA. oNaPi-IIc siRNA also suppressed Na
+
/H
+
exchanger regulatory factor 1 expression in OK cells.
Conclusion
These findings suggest that NaPi-IIc is important for the expression of NaPi-IIa (NaPi-4) protein in OK cells. Suppression of Npt2c may downregulate Npt2a function in HHRH patients.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Cells, Cultured</subject><subject>Clonal deletion</subject><subject>Cloning</subject><subject>Familial Hypophosphatemic Rickets - etiology</subject><subject>Humans</subject><subject>Hypercalciuria</subject><subject>Hypercalciuria - etiology</subject><subject>Hypophosphatemia</subject><subject>Kidney - metabolism</subject><subject>Kidneys</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>mRNA</subject><subject>Na+/H+-exchanging ATPase</subject><subject>Nephrology</subject><subject>Opossums</subject><subject>Original Article</subject><subject>Phosphate Transport Proteins - physiology</subject><subject>Phosphate transporter</subject><subject>Phosphates - metabolism</subject><subject>Proteins</subject><subject>Reabsorption</subject><subject>Rickets</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA-mediated interference</subject><subject>siRNA</subject><subject>Sodium</subject><subject>Sodium-Phosphate Cotransporter Proteins, Type IIc - physiology</subject><subject>Urology</subject><subject>Xenopus laevis</subject><issn>1342-1751</issn><issn>1437-7799</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkU9P3DAQxa0KVOi2H6CXyhKXXgz-E8fxESFKV0ItB3q2nPWENU3sYDuH_fZ4tYuQOL2R5qc3o_cQ-s7oJaNUXWVGmVSEso6wVgrSfELnrBGKKKX1SZ1FwwlTkp2hLzk_U0o7LfVndCaoYKpp1Dkq18GOu-wzjgOOc8x5mfB_7wLs8B_74Ml6vcE5Or9MxMEMwUEoeN7GPG9tAVySDXmOqUDCJeKl7lMuNjj84PG26ujDE_YBb5fJhqPzV3Q62DHDt6Ou0L9ft483v8n937v1zfU9mTnjhWg9OGgHzUENff3YspZLp60UneaK9iBZxwAGvelb1ruu23AOXEnVSweia8UK_Tz4zim-LJCLmXzewDjaAHHJpl6hnLY1iopefECf45JqNnuKadpQVUNboR9HaukncGZOfrJpZ97yrAA_ALmuwhOkdxtGzb40cyjN1NLMvjTTiFcCvYgT</recordid><startdate>20190301</startdate><enddate>20190301</enddate><creator>Fujii, Toru</creator><creator>Shiozaki, Yuji</creator><creator>Segawa, Hiroko</creator><creator>Nishiguchi, Shiori</creator><creator>Hanazaki, Ai</creator><creator>Noguchi, Miwa</creator><creator>Kirino, Ruri</creator><creator>Sasaki, Sumire</creator><creator>Tanifuji, Kazuya</creator><creator>Koike, Megumi</creator><creator>Yokoyama, Mizuki</creator><creator>Arima, Yuki</creator><creator>Kaneko, Ichiro</creator><creator>Tatsumi, Sawako</creator><creator>Ito, Mikiko</creator><creator>Miyamoto, Ken-ichi</creator><general>Springer Singapore</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QP</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0905-246X</orcidid></search><sort><creationdate>20190301</creationdate><title>Analysis of opossum kidney NaPi-IIc sodium-dependent phosphate transporter to understand Pi handling in human kidney</title><author>Fujii, Toru ; Shiozaki, Yuji ; Segawa, Hiroko ; Nishiguchi, Shiori ; Hanazaki, Ai ; Noguchi, Miwa ; Kirino, Ruri ; Sasaki, Sumire ; Tanifuji, Kazuya ; Koike, Megumi ; Yokoyama, Mizuki ; Arima, Yuki ; Kaneko, Ichiro ; Tatsumi, Sawako ; Ito, Mikiko ; Miyamoto, Ken-ichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p212t-99fde6f92e7fb031a1625d9a5389270be5181eef9cb61bd88c22e2757b5de3863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Cells, Cultured</topic><topic>Clonal deletion</topic><topic>Cloning</topic><topic>Familial Hypophosphatemic Rickets - etiology</topic><topic>Humans</topic><topic>Hypercalciuria</topic><topic>Hypercalciuria - etiology</topic><topic>Hypophosphatemia</topic><topic>Kidney - metabolism</topic><topic>Kidneys</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>mRNA</topic><topic>Na+/H+-exchanging ATPase</topic><topic>Nephrology</topic><topic>Opossums</topic><topic>Original Article</topic><topic>Phosphate Transport Proteins - physiology</topic><topic>Phosphate transporter</topic><topic>Phosphates - metabolism</topic><topic>Proteins</topic><topic>Reabsorption</topic><topic>Rickets</topic><topic>RNA, Small Interfering - genetics</topic><topic>RNA-mediated interference</topic><topic>siRNA</topic><topic>Sodium</topic><topic>Sodium-Phosphate Cotransporter Proteins, Type IIc - physiology</topic><topic>Urology</topic><topic>Xenopus laevis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fujii, Toru</creatorcontrib><creatorcontrib>Shiozaki, Yuji</creatorcontrib><creatorcontrib>Segawa, Hiroko</creatorcontrib><creatorcontrib>Nishiguchi, Shiori</creatorcontrib><creatorcontrib>Hanazaki, Ai</creatorcontrib><creatorcontrib>Noguchi, Miwa</creatorcontrib><creatorcontrib>Kirino, Ruri</creatorcontrib><creatorcontrib>Sasaki, Sumire</creatorcontrib><creatorcontrib>Tanifuji, Kazuya</creatorcontrib><creatorcontrib>Koike, Megumi</creatorcontrib><creatorcontrib>Yokoyama, Mizuki</creatorcontrib><creatorcontrib>Arima, Yuki</creatorcontrib><creatorcontrib>Kaneko, Ichiro</creatorcontrib><creatorcontrib>Tatsumi, Sawako</creatorcontrib><creatorcontrib>Ito, Mikiko</creatorcontrib><creatorcontrib>Miyamoto, Ken-ichi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fujii, Toru</au><au>Shiozaki, Yuji</au><au>Segawa, Hiroko</au><au>Nishiguchi, Shiori</au><au>Hanazaki, Ai</au><au>Noguchi, Miwa</au><au>Kirino, Ruri</au><au>Sasaki, Sumire</au><au>Tanifuji, Kazuya</au><au>Koike, Megumi</au><au>Yokoyama, Mizuki</au><au>Arima, Yuki</au><au>Kaneko, Ichiro</au><au>Tatsumi, Sawako</au><au>Ito, Mikiko</au><au>Miyamoto, Ken-ichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of opossum kidney NaPi-IIc sodium-dependent phosphate transporter to understand Pi handling in human kidney</atitle><jtitle>Clinical and experimental nephrology</jtitle><stitle>Clin Exp Nephrol</stitle><addtitle>Clin Exp Nephrol</addtitle><date>2019-03-01</date><risdate>2019</risdate><volume>23</volume><issue>3</issue><spage>313</spage><epage>324</epage><pages>313-324</pages><issn>1342-1751</issn><eissn>1437-7799</eissn><abstract>Background
The role of Na
+
-dependent inorganic phosphate (Pi) transporters in the human kidney is not fully clarified. Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is caused by loss-of-function mutations in the IIc Na
+
-dependent Pi transporter (NPT2c/Npt2c/NaPi-IIc) gene. Another Na
+
-dependent type II transporter, (NPT2A/Npt2a/NaPi-IIa), is also important for renal Pi reabsorption in humans. In mice, Npt2c deletion does not lead to hypophosphatemia and rickets because Npt2a compensates for the impaired Pi reabsorption. To clarify the differences between mouse and human, we investigated the relation between NaPi-IIa and NaPi-IIc functions in opossum kidney (OK) cells.
Methods
We cloned NaPi-IIc from OK cells and created opossum NaPi-IIc (oNaPi-IIc) antibodies. We used oNaPi-IIc small interference (si)RNA and investigated the role of NaPi-IIc in Pi transport in OK cells.
Results
We cloned opossum kidney NaPi-IIc cDNAs encoding 622 amino acid proteins (variant1) and examined their pH- and sodium-dependency. The antibodies reacted specifically with 75-kDa and 150-kDa protein bands, and the siRNA of NaPi-IIc markedly suppressed endogenous oNaPi-IIc in OK cells. Treatment with siRNA significantly suppressed the expression of NaPi-4 (NaPi-IIa) protein and mRNA. oNaPi-IIc siRNA also suppressed Na
+
/H
+
exchanger regulatory factor 1 expression in OK cells.
Conclusion
These findings suggest that NaPi-IIc is important for the expression of NaPi-IIa (NaPi-4) protein in OK cells. Suppression of Npt2c may downregulate Npt2a function in HHRH patients.</abstract><cop>Singapore</cop><pub>Springer Singapore</pub><pmid>30317447</pmid><doi>10.1007/s10157-018-1653-4</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-0905-246X</orcidid></addata></record> |
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| ispartof | Clinical and experimental nephrology, 2019-03, Vol.23 (3), p.313-324 |
| issn | 1342-1751 1437-7799 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals Antibodies Cells, Cultured Clonal deletion Cloning Familial Hypophosphatemic Rickets - etiology Humans Hypercalciuria Hypercalciuria - etiology Hypophosphatemia Kidney - metabolism Kidneys Medicine Medicine & Public Health Mice mRNA Na+/H+-exchanging ATPase Nephrology Opossums Original Article Phosphate Transport Proteins - physiology Phosphate transporter Phosphates - metabolism Proteins Reabsorption Rickets RNA, Small Interfering - genetics RNA-mediated interference siRNA Sodium Sodium-Phosphate Cotransporter Proteins, Type IIc - physiology Urology Xenopus laevis |
| title | Analysis of opossum kidney NaPi-IIc sodium-dependent phosphate transporter to understand Pi handling in human kidney |
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