Decreased KLHL3 expression is involved in the activation of WNK-OSR1/SPAK-NCC cascade in type 1 diabetic mice
Familial hyperkalemic hypertension (FHHt; also called pseudohypoaldosteronism type II) is a hereditary hypertensive disease which can be caused by mutations in four genes: WNK1 [with no lysine (K) 1], WNK4 , Kelch-like3 (KLHL3), and cullin3 (CUL3). Decreased KLHL3 expression was identified as being...
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| Veröffentlicht in: | Pflügers Archiv 2021-02, Vol.473 (2), p.185-196 |
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| description | Familial hyperkalemic hypertension (FHHt; also called pseudohypoaldosteronism type II) is a hereditary hypertensive disease which can be caused by mutations in four genes:
WNK1
[with no lysine (K) 1],
WNK4
,
Kelch-like3
(KLHL3), and
cullin3
(CUL3). Decreased KLHL3 expression was identified as being involved in the pathogenesis of FHHt caused by cullin 3 disease mutations. Recent studies have revealed an increased WNK4 and hence Na-Cl cotransporter (NCC) activity in the db/db mice, resulting from PKC-mediated KLHL3 phosphorylation, which impairs the degradation of its substrate, WNK4. However, whether WNK4 and NCC were activated in type 1 diabetes still remains unclear. We created streptozotocin-induced type 1 diabetic mice and revealed that renal WNK-oxidative stress response kinase-1/STE20/SPS1-related proline alanine–rich kinase (OSR1/SPAK)-NCC cascade was activated, whereas KLHL3 expression was markedly decreased and CUL3 was heavily neddylated. Moreover, decreased KLHL3 was reversed and WNK1 and WNK4 abundance increased by MLN4924, a neddylation inhibitor. In vitro, our study also showed decreased KLHL3 abundance without any significant change in phosphorylated KLHL3 under high glucose exposure. These results indicate that decreased KLHL3 likely plays a role in the pathogenesis of renal sodium reabsorption in hyperglycemic conditions. |
| doi_str_mv | 10.1007/s00424-020-02509-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2480547135</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2480547135</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-c87851639ab1ba794d6a4931cdd1778f590fe984d16d7e852edadbadbd277ce53</originalsourceid><addsrcrecordid>eNp9kEtPGzEURq2qqATaP9AFstS14foxY88SpbyUCFBp1aXlse8UIzKT2pMI_j0O4bFD8pUX37nflQ4h3zkccgB9lAGUUAwElKmgYeYTmXAlBRPA5WcyAZCc1bo2u2Qv5zsAEMqIL2RXykIpUU3I4if6hC5joLP5-VxSfFgmzDkOPY2Zxn493K9LGHs63iJ1foxrN27SoaN_L2fs6uYXP7q5Pp6xy-mUepe9C_iMPy6Rchqia3GMni6ix69kp3P3Gb-9_Pvkz-nJ7-k5m1-dXUyP58xLXY3MG20qXsvGtbx1ulGhdqqR3IfAtTZd1UCHjVGB10GjqQQGF9rygtDaYyX3yY9t7zIN_1eYR3s3rFJfTtpiACqludxQYkv5NOScsLPLFBcuPVoOdmPYbg3bYtg-G7amLB28VK_aBYa3lVelBZBbIJeo_4fp_fYHtU_Xk4Rw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2480547135</pqid></control><display><type>article</type><title>Decreased KLHL3 expression is involved in the activation of WNK-OSR1/SPAK-NCC cascade in type 1 diabetic mice</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Guo, Qin ; Zhang, Ya ; Jiang, Geng-Ru ; Zhang, Chong</creator><creatorcontrib>Guo, Qin ; Zhang, Ya ; Jiang, Geng-Ru ; Zhang, Chong</creatorcontrib><description>Familial hyperkalemic hypertension (FHHt; also called pseudohypoaldosteronism type II) is a hereditary hypertensive disease which can be caused by mutations in four genes:
WNK1
[with no lysine (K) 1],
WNK4
,
Kelch-like3
(KLHL3), and
cullin3
(CUL3). Decreased KLHL3 expression was identified as being involved in the pathogenesis of FHHt caused by cullin 3 disease mutations. Recent studies have revealed an increased WNK4 and hence Na-Cl cotransporter (NCC) activity in the db/db mice, resulting from PKC-mediated KLHL3 phosphorylation, which impairs the degradation of its substrate, WNK4. However, whether WNK4 and NCC were activated in type 1 diabetes still remains unclear. We created streptozotocin-induced type 1 diabetic mice and revealed that renal WNK-oxidative stress response kinase-1/STE20/SPS1-related proline alanine–rich kinase (OSR1/SPAK)-NCC cascade was activated, whereas KLHL3 expression was markedly decreased and CUL3 was heavily neddylated. Moreover, decreased KLHL3 was reversed and WNK1 and WNK4 abundance increased by MLN4924, a neddylation inhibitor. In vitro, our study also showed decreased KLHL3 abundance without any significant change in phosphorylated KLHL3 under high glucose exposure. These results indicate that decreased KLHL3 likely plays a role in the pathogenesis of renal sodium reabsorption in hyperglycemic conditions.</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s00424-020-02509-8</identifier><identifier>PMID: 33432425</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Abundance ; Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; Alanine ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Blood Glucose - metabolism ; Blood Pressure ; Cell Biology ; Cullin ; Cullin Proteins - metabolism ; Diabetes ; Diabetes mellitus (insulin dependent) ; Diabetes Mellitus, Experimental - chemically induced ; Diabetes Mellitus, Experimental - genetics ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - physiopathology ; Diabetes Mellitus, Type 1 - chemically induced ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 1 - physiopathology ; HEK293 Cells ; Human Physiology ; Humans ; Ion Channels ; Kidney - metabolism ; Kidney - physiopathology ; Lysine ; Male ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins - genetics ; Microfilament Proteins - metabolism ; Molecular Medicine ; Mutation ; Neurosciences ; Oxidative stress ; Pathogenesis ; Phosphorylation ; Proline ; Protein kinase C ; Protein Serine-Threonine Kinases - genetics ; Protein Serine-Threonine Kinases - metabolism ; Pseudohypoaldosteronism ; Reabsorption ; Receptors ; Receptors and Transporters ; Renal Reabsorption ; Signal Transduction ; Sodium ; Sodium - metabolism ; Solute Carrier Family 12, Member 3 - metabolism ; Streptozocin ; Ubiquitination ; WNK Lysine-Deficient Protein Kinase 1 - genetics ; WNK Lysine-Deficient Protein Kinase 1 - metabolism</subject><ispartof>Pflügers Archiv, 2021-02, Vol.473 (2), p.185-196</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH, DE part of Springer Nature 2021</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH, DE part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-c87851639ab1ba794d6a4931cdd1778f590fe984d16d7e852edadbadbd277ce53</citedby><cites>FETCH-LOGICAL-c375t-c87851639ab1ba794d6a4931cdd1778f590fe984d16d7e852edadbadbd277ce53</cites><orcidid>0000-0002-3590-6211</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/s00424-020-02509-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00424-020-02509-8$$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/33432425$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Qin</creatorcontrib><creatorcontrib>Zhang, Ya</creatorcontrib><creatorcontrib>Jiang, Geng-Ru</creatorcontrib><creatorcontrib>Zhang, Chong</creatorcontrib><title>Decreased KLHL3 expression is involved in the activation of WNK-OSR1/SPAK-NCC cascade in type 1 diabetic mice</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch - Eur J Physiol</addtitle><addtitle>Pflugers Arch</addtitle><description>Familial hyperkalemic hypertension (FHHt; also called pseudohypoaldosteronism type II) is a hereditary hypertensive disease which can be caused by mutations in four genes:
WNK1
[with no lysine (K) 1],
WNK4
,
Kelch-like3
(KLHL3), and
cullin3
(CUL3). Decreased KLHL3 expression was identified as being involved in the pathogenesis of FHHt caused by cullin 3 disease mutations. Recent studies have revealed an increased WNK4 and hence Na-Cl cotransporter (NCC) activity in the db/db mice, resulting from PKC-mediated KLHL3 phosphorylation, which impairs the degradation of its substrate, WNK4. However, whether WNK4 and NCC were activated in type 1 diabetes still remains unclear. We created streptozotocin-induced type 1 diabetic mice and revealed that renal WNK-oxidative stress response kinase-1/STE20/SPS1-related proline alanine–rich kinase (OSR1/SPAK)-NCC cascade was activated, whereas KLHL3 expression was markedly decreased and CUL3 was heavily neddylated. Moreover, decreased KLHL3 was reversed and WNK1 and WNK4 abundance increased by MLN4924, a neddylation inhibitor. In vitro, our study also showed decreased KLHL3 abundance without any significant change in phosphorylated KLHL3 under high glucose exposure. These results indicate that decreased KLHL3 likely plays a role in the pathogenesis of renal sodium reabsorption in hyperglycemic conditions.</description><subject>Abundance</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Alanine</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood Glucose - metabolism</subject><subject>Blood Pressure</subject><subject>Cell Biology</subject><subject>Cullin</subject><subject>Cullin Proteins - metabolism</subject><subject>Diabetes</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Diabetes Mellitus, Experimental - chemically induced</subject><subject>Diabetes Mellitus, Experimental - genetics</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Diabetes Mellitus, Type 1 - chemically induced</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 1 - physiopathology</subject><subject>HEK293 Cells</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Ion Channels</subject><subject>Kidney - metabolism</subject><subject>Kidney - physiopathology</subject><subject>Lysine</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microfilament Proteins - genetics</subject><subject>Microfilament Proteins - metabolism</subject><subject>Molecular Medicine</subject><subject>Mutation</subject><subject>Neurosciences</subject><subject>Oxidative stress</subject><subject>Pathogenesis</subject><subject>Phosphorylation</subject><subject>Proline</subject><subject>Protein kinase C</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Protein Serine-Threonine Kinases - metabolism</subject><subject>Pseudohypoaldosteronism</subject><subject>Reabsorption</subject><subject>Receptors</subject><subject>Receptors and Transporters</subject><subject>Renal Reabsorption</subject><subject>Signal Transduction</subject><subject>Sodium</subject><subject>Sodium - metabolism</subject><subject>Solute Carrier Family 12, Member 3 - metabolism</subject><subject>Streptozocin</subject><subject>Ubiquitination</subject><subject>WNK Lysine-Deficient Protein Kinase 1 - genetics</subject><subject>WNK Lysine-Deficient Protein Kinase 1 - metabolism</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kEtPGzEURq2qqATaP9AFstS14foxY88SpbyUCFBp1aXlse8UIzKT2pMI_j0O4bFD8pUX37nflQ4h3zkccgB9lAGUUAwElKmgYeYTmXAlBRPA5WcyAZCc1bo2u2Qv5zsAEMqIL2RXykIpUU3I4if6hC5joLP5-VxSfFgmzDkOPY2Zxn493K9LGHs63iJ1foxrN27SoaN_L2fs6uYXP7q5Pp6xy-mUepe9C_iMPy6Rchqia3GMni6ix69kp3P3Gb-9_Pvkz-nJ7-k5m1-dXUyP58xLXY3MG20qXsvGtbx1ulGhdqqR3IfAtTZd1UCHjVGB10GjqQQGF9rygtDaYyX3yY9t7zIN_1eYR3s3rFJfTtpiACqludxQYkv5NOScsLPLFBcuPVoOdmPYbg3bYtg-G7amLB28VK_aBYa3lVelBZBbIJeo_4fp_fYHtU_Xk4Rw</recordid><startdate>20210201</startdate><enddate>20210201</enddate><creator>Guo, Qin</creator><creator>Zhang, Ya</creator><creator>Jiang, Geng-Ru</creator><creator>Zhang, Chong</creator><general>Springer Berlin Heidelberg</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>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><orcidid>https://orcid.org/0000-0002-3590-6211</orcidid></search><sort><creationdate>20210201</creationdate><title>Decreased KLHL3 expression is involved in the activation of WNK-OSR1/SPAK-NCC cascade in type 1 diabetic mice</title><author>Guo, Qin ; Zhang, Ya ; Jiang, Geng-Ru ; Zhang, Chong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-c87851639ab1ba794d6a4931cdd1778f590fe984d16d7e852edadbadbd277ce53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Abundance</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Alanine</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood Glucose - metabolism</topic><topic>Blood Pressure</topic><topic>Cell Biology</topic><topic>Cullin</topic><topic>Cullin Proteins - metabolism</topic><topic>Diabetes</topic><topic>Diabetes mellitus (insulin dependent)</topic><topic>Diabetes Mellitus, Experimental - chemically induced</topic><topic>Diabetes Mellitus, Experimental - genetics</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Diabetes Mellitus, Type 1 - chemically induced</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Diabetes Mellitus, Type 1 - physiopathology</topic><topic>HEK293 Cells</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Ion Channels</topic><topic>Kidney - metabolism</topic><topic>Kidney - physiopathology</topic><topic>Lysine</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microfilament Proteins - genetics</topic><topic>Microfilament Proteins - metabolism</topic><topic>Molecular Medicine</topic><topic>Mutation</topic><topic>Neurosciences</topic><topic>Oxidative stress</topic><topic>Pathogenesis</topic><topic>Phosphorylation</topic><topic>Proline</topic><topic>Protein kinase C</topic><topic>Protein Serine-Threonine Kinases - genetics</topic><topic>Protein Serine-Threonine Kinases - metabolism</topic><topic>Pseudohypoaldosteronism</topic><topic>Reabsorption</topic><topic>Receptors</topic><topic>Receptors and Transporters</topic><topic>Renal Reabsorption</topic><topic>Signal Transduction</topic><topic>Sodium</topic><topic>Sodium - metabolism</topic><topic>Solute Carrier Family 12, Member 3 - metabolism</topic><topic>Streptozocin</topic><topic>Ubiquitination</topic><topic>WNK Lysine-Deficient Protein Kinase 1 - genetics</topic><topic>WNK Lysine-Deficient Protein Kinase 1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Qin</creatorcontrib><creatorcontrib>Zhang, Ya</creatorcontrib><creatorcontrib>Jiang, Geng-Ru</creatorcontrib><creatorcontrib>Zhang, Chong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><jtitle>Pflügers Archiv</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Qin</au><au>Zhang, Ya</au><au>Jiang, Geng-Ru</au><au>Zhang, Chong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decreased KLHL3 expression is involved in the activation of WNK-OSR1/SPAK-NCC cascade in type 1 diabetic mice</atitle><jtitle>Pflügers Archiv</jtitle><stitle>Pflugers Arch - Eur J Physiol</stitle><addtitle>Pflugers Arch</addtitle><date>2021-02-01</date><risdate>2021</risdate><volume>473</volume><issue>2</issue><spage>185</spage><epage>196</epage><pages>185-196</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>Familial hyperkalemic hypertension (FHHt; also called pseudohypoaldosteronism type II) is a hereditary hypertensive disease which can be caused by mutations in four genes:
WNK1
[with no lysine (K) 1],
WNK4
,
Kelch-like3
(KLHL3), and
cullin3
(CUL3). Decreased KLHL3 expression was identified as being involved in the pathogenesis of FHHt caused by cullin 3 disease mutations. Recent studies have revealed an increased WNK4 and hence Na-Cl cotransporter (NCC) activity in the db/db mice, resulting from PKC-mediated KLHL3 phosphorylation, which impairs the degradation of its substrate, WNK4. However, whether WNK4 and NCC were activated in type 1 diabetes still remains unclear. We created streptozotocin-induced type 1 diabetic mice and revealed that renal WNK-oxidative stress response kinase-1/STE20/SPS1-related proline alanine–rich kinase (OSR1/SPAK)-NCC cascade was activated, whereas KLHL3 expression was markedly decreased and CUL3 was heavily neddylated. Moreover, decreased KLHL3 was reversed and WNK1 and WNK4 abundance increased by MLN4924, a neddylation inhibitor. In vitro, our study also showed decreased KLHL3 abundance without any significant change in phosphorylated KLHL3 under high glucose exposure. These results indicate that decreased KLHL3 likely plays a role in the pathogenesis of renal sodium reabsorption in hyperglycemic conditions.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>33432425</pmid><doi>10.1007/s00424-020-02509-8</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-3590-6211</orcidid></addata></record> |
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| ispartof | Pflügers Archiv, 2021-02, Vol.473 (2), p.185-196 |
| issn | 0031-6768 1432-2013 |
| language | eng |
| recordid | cdi_proquest_journals_2480547135 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Abundance Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Alanine Animals Biomedical and Life Sciences Biomedicine Blood Glucose - metabolism Blood Pressure Cell Biology Cullin Cullin Proteins - metabolism Diabetes Diabetes mellitus (insulin dependent) Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - physiopathology Diabetes Mellitus, Type 1 - chemically induced Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 1 - physiopathology HEK293 Cells Human Physiology Humans Ion Channels Kidney - metabolism Kidney - physiopathology Lysine Male Mice Mice, Inbred C57BL Microfilament Proteins - genetics Microfilament Proteins - metabolism Molecular Medicine Mutation Neurosciences Oxidative stress Pathogenesis Phosphorylation Proline Protein kinase C Protein Serine-Threonine Kinases - genetics Protein Serine-Threonine Kinases - metabolism Pseudohypoaldosteronism Reabsorption Receptors Receptors and Transporters Renal Reabsorption Signal Transduction Sodium Sodium - metabolism Solute Carrier Family 12, Member 3 - metabolism Streptozocin Ubiquitination WNK Lysine-Deficient Protein Kinase 1 - genetics WNK Lysine-Deficient Protein Kinase 1 - metabolism |
| title | Decreased KLHL3 expression is involved in the activation of WNK-OSR1/SPAK-NCC cascade in type 1 diabetic mice |
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