Progressive Myoclonic Epilepsy-Associated Gene KCTD7 is a Regulator of Potassium Conductance in Neurons
The potassium channel tetramerization domain-containing protein 7 (KCTD7) was named after the structural homology of its predicted N-terminal broad complex, tramtrack and bric à brac/poxvirus and zinc finger domain with the T1 domain of the Kv potassium channel, but its expression profile and cellul...
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Veröffentlicht in: | Molecular neurobiology 2011-08, Vol.44 (1), p.111-121 |
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creator | Azizieh, Régis Orduz, David Van Bogaert, Patrick Bouschet, Tristan Rodriguez, Wendy Schiffmann, Serge N. Pirson, Isabelle Abramowicz, Marc J. |
description | The potassium channel tetramerization domain-containing protein 7 (KCTD7) was named after the structural homology of its predicted N-terminal broad complex, tramtrack and bric à brac/poxvirus and zinc finger domain with the T1 domain of the Kv potassium channel, but its expression profile and cellular function are still largely unknown. We have recently reported a homozygous nonsense mutation of
KCTD7
in patients with a novel form of autosomal recessive progressive myoclonic epilepsy. Here, we show that KCTD7 expression hyperpolarizes the cell membrane and reduces the excitability of transfected neurons in patch clamp experiments. We found the expression of KCTD7 in the hippocampal and Purkinje cells of the murine brain, an expression profile consistent with our patients’ phenotype. The effect on the plasma membrane resting potential is possibly mediated by Cullin-3, as we demonstrated direct molecular interaction of KCTD7 with Cullin-3 in co-immunoprecipitation assays. Our data link progressive myoclonic epilepsy to an inherited defect of the neuron plasma membrane’s resting potential in the brain. |
doi_str_mv | 10.1007/s12035-011-8194-0 |
format | Article |
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KCTD7
in patients with a novel form of autosomal recessive progressive myoclonic epilepsy. Here, we show that KCTD7 expression hyperpolarizes the cell membrane and reduces the excitability of transfected neurons in patch clamp experiments. We found the expression of KCTD7 in the hippocampal and Purkinje cells of the murine brain, an expression profile consistent with our patients’ phenotype. The effect on the plasma membrane resting potential is possibly mediated by Cullin-3, as we demonstrated direct molecular interaction of KCTD7 with Cullin-3 in co-immunoprecipitation assays. Our data link progressive myoclonic epilepsy to an inherited defect of the neuron plasma membrane’s resting potential in the brain.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-011-8194-0</identifier><identifier>PMID: 21710140</identifier><language>eng</language><publisher>New York: Humana Press Inc</publisher><subject>Action Potentials - physiology ; Animals ; Antibody Specificity ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell membranes ; Cells, Cultured ; Cercopithecus aethiops ; COS Cells ; Cullin ; Cullin Proteins - metabolism ; Epilepsy ; Excitability ; Gene Expression Regulation ; Genes ; Hippocampus ; Hippocampus - metabolism ; Hippocampus - pathology ; Homology ; Humans ; Immunoprecipitation ; Ion Channel Gating - genetics ; Membrane potential ; Mice ; Myoclonic Epilepsies, Progressive - genetics ; Neurobiology ; Neurology ; Neurons ; Neurons - metabolism ; Neurons - pathology ; Neurosciences ; Nonsense mutation ; Olfactory Bulb - metabolism ; Olfactory Bulb - pathology ; Phenotypes ; Potassium ; Potassium Channels - genetics ; Potassium Channels - metabolism ; Potassium conductance ; Poxvirus ; Protein Binding ; Protein Multimerization ; Protein Transport ; Purkinje cells ; Purkinje Cells - metabolism ; Purkinje Cells - pathology ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Zinc finger proteins</subject><ispartof>Molecular neurobiology, 2011-08, Vol.44 (1), p.111-121</ispartof><rights>Springer Science+Business Media, LLC 2011</rights><rights>Springer Science+Business Media, LLC 2011.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-e4074578f0c455881ea9316a239fa139c64c092deafd6cc0528a931ac8a73b7b3</citedby><cites>FETCH-LOGICAL-c496t-e4074578f0c455881ea9316a239fa139c64c092deafd6cc0528a931ac8a73b7b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-011-8194-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-011-8194-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21710140$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Azizieh, Régis</creatorcontrib><creatorcontrib>Orduz, David</creatorcontrib><creatorcontrib>Van Bogaert, Patrick</creatorcontrib><creatorcontrib>Bouschet, Tristan</creatorcontrib><creatorcontrib>Rodriguez, Wendy</creatorcontrib><creatorcontrib>Schiffmann, Serge N.</creatorcontrib><creatorcontrib>Pirson, Isabelle</creatorcontrib><creatorcontrib>Abramowicz, Marc J.</creatorcontrib><title>Progressive Myoclonic Epilepsy-Associated Gene KCTD7 is a Regulator of Potassium Conductance in Neurons</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>The potassium channel tetramerization domain-containing protein 7 (KCTD7) was named after the structural homology of its predicted N-terminal broad complex, tramtrack and bric à brac/poxvirus and zinc finger domain with the T1 domain of the Kv potassium channel, but its expression profile and cellular function are still largely unknown. We have recently reported a homozygous nonsense mutation of
KCTD7
in patients with a novel form of autosomal recessive progressive myoclonic epilepsy. Here, we show that KCTD7 expression hyperpolarizes the cell membrane and reduces the excitability of transfected neurons in patch clamp experiments. We found the expression of KCTD7 in the hippocampal and Purkinje cells of the murine brain, an expression profile consistent with our patients’ phenotype. The effect on the plasma membrane resting potential is possibly mediated by Cullin-3, as we demonstrated direct molecular interaction of KCTD7 with Cullin-3 in co-immunoprecipitation assays. Our data link progressive myoclonic epilepsy to an inherited defect of the neuron plasma membrane’s resting potential in the brain.</description><subject>Action Potentials - physiology</subject><subject>Animals</subject><subject>Antibody Specificity</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell membranes</subject><subject>Cells, Cultured</subject><subject>Cercopithecus aethiops</subject><subject>COS Cells</subject><subject>Cullin</subject><subject>Cullin Proteins - metabolism</subject><subject>Epilepsy</subject><subject>Excitability</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Homology</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Ion Channel Gating - genetics</subject><subject>Membrane potential</subject><subject>Mice</subject><subject>Myoclonic Epilepsies, Progressive - genetics</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neurosciences</subject><subject>Nonsense mutation</subject><subject>Olfactory Bulb - metabolism</subject><subject>Olfactory Bulb - pathology</subject><subject>Phenotypes</subject><subject>Potassium</subject><subject>Potassium Channels - genetics</subject><subject>Potassium Channels - metabolism</subject><subject>Potassium conductance</subject><subject>Poxvirus</subject><subject>Protein Binding</subject><subject>Protein Multimerization</subject><subject>Protein Transport</subject><subject>Purkinje cells</subject><subject>Purkinje Cells - metabolism</subject><subject>Purkinje Cells - pathology</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Zinc finger proteins</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</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>eNqFkU1v1DAQhi1ERbeFH8AFWXDoKWXGdvxxrJZSUAtUqJwjrzNZpcrGi50g7b-vV1tAQqo4zWGeeWdGD2OvEc4RwLzPKEDWFSBWFp2q4BlbYF27CtGK52wB1snKaGWP2UnO9wBCIJgX7FigQUAFC7a-TXGdKOf-F_EvuxiGOPaBX277gbZ5V13kHEPvJ2r5FY3Er5d3HwzvM_f8O63nwU8x8djx2zj5EjJv-DKO7RwmPwbi_ci_0pzimF-yo84PmV491lP24-Pl3fJTdfPt6vPy4qYKyumpIgVG1cZ2EFRdW4vknUTthXSdR-mCVgGcaMl3rQ4BamH3gA_WG7kyK3nKzg652xR_zpSnZtPnQMPgR4pzbqyVoLRz4v-k0eignFDIt_-Q93FOY3mjQLUWQktdoHdPQUK78pIB3C_FAxVSzDlR12xTv_Fp1yA0e6fNwWlTnDZ7pw2UmTePyfNqQ-2fid8SCyAOQC6tcU3p7-qnUx8AxWWqDQ</recordid><startdate>20110801</startdate><enddate>20110801</enddate><creator>Azizieh, Régis</creator><creator>Orduz, David</creator><creator>Van Bogaert, Patrick</creator><creator>Bouschet, Tristan</creator><creator>Rodriguez, Wendy</creator><creator>Schiffmann, Serge N.</creator><creator>Pirson, Isabelle</creator><creator>Abramowicz, Marc J.</creator><general>Humana Press Inc</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>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</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>FR3</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>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>7T7</scope><scope>C1K</scope><scope>RC3</scope></search><sort><creationdate>20110801</creationdate><title>Progressive Myoclonic Epilepsy-Associated Gene KCTD7 is a Regulator of Potassium Conductance in Neurons</title><author>Azizieh, Régis ; Orduz, David ; Van Bogaert, Patrick ; Bouschet, Tristan ; Rodriguez, Wendy ; Schiffmann, Serge N. ; Pirson, Isabelle ; Abramowicz, Marc J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-e4074578f0c455881ea9316a239fa139c64c092deafd6cc0528a931ac8a73b7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Action Potentials - physiology</topic><topic>Animals</topic><topic>Antibody Specificity</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell membranes</topic><topic>Cells, Cultured</topic><topic>Cercopithecus aethiops</topic><topic>COS Cells</topic><topic>Cullin</topic><topic>Cullin Proteins - metabolism</topic><topic>Epilepsy</topic><topic>Excitability</topic><topic>Gene Expression Regulation</topic><topic>Genes</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>Homology</topic><topic>Humans</topic><topic>Immunoprecipitation</topic><topic>Ion Channel Gating - genetics</topic><topic>Membrane potential</topic><topic>Mice</topic><topic>Myoclonic Epilepsies, Progressive - genetics</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurons</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Neurosciences</topic><topic>Nonsense mutation</topic><topic>Olfactory Bulb - metabolism</topic><topic>Olfactory Bulb - pathology</topic><topic>Phenotypes</topic><topic>Potassium</topic><topic>Potassium Channels - genetics</topic><topic>Potassium Channels - metabolism</topic><topic>Potassium conductance</topic><topic>Poxvirus</topic><topic>Protein Binding</topic><topic>Protein Multimerization</topic><topic>Protein Transport</topic><topic>Purkinje cells</topic><topic>Purkinje Cells - metabolism</topic><topic>Purkinje Cells - pathology</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Zinc finger proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Azizieh, Régis</creatorcontrib><creatorcontrib>Orduz, David</creatorcontrib><creatorcontrib>Van Bogaert, Patrick</creatorcontrib><creatorcontrib>Bouschet, Tristan</creatorcontrib><creatorcontrib>Rodriguez, Wendy</creatorcontrib><creatorcontrib>Schiffmann, Serge N.</creatorcontrib><creatorcontrib>Pirson, Isabelle</creatorcontrib><creatorcontrib>Abramowicz, Marc J.</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</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>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>Engineering Research Database</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>ProQuest Psychology</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Genetics Abstracts</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Azizieh, Régis</au><au>Orduz, David</au><au>Van Bogaert, Patrick</au><au>Bouschet, Tristan</au><au>Rodriguez, Wendy</au><au>Schiffmann, Serge N.</au><au>Pirson, Isabelle</au><au>Abramowicz, Marc J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Progressive Myoclonic Epilepsy-Associated Gene KCTD7 is a Regulator of Potassium Conductance in Neurons</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2011-08-01</date><risdate>2011</risdate><volume>44</volume><issue>1</issue><spage>111</spage><epage>121</epage><pages>111-121</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>The potassium channel tetramerization domain-containing protein 7 (KCTD7) was named after the structural homology of its predicted N-terminal broad complex, tramtrack and bric à brac/poxvirus and zinc finger domain with the T1 domain of the Kv potassium channel, but its expression profile and cellular function are still largely unknown. We have recently reported a homozygous nonsense mutation of
KCTD7
in patients with a novel form of autosomal recessive progressive myoclonic epilepsy. Here, we show that KCTD7 expression hyperpolarizes the cell membrane and reduces the excitability of transfected neurons in patch clamp experiments. We found the expression of KCTD7 in the hippocampal and Purkinje cells of the murine brain, an expression profile consistent with our patients’ phenotype. The effect on the plasma membrane resting potential is possibly mediated by Cullin-3, as we demonstrated direct molecular interaction of KCTD7 with Cullin-3 in co-immunoprecipitation assays. Our data link progressive myoclonic epilepsy to an inherited defect of the neuron plasma membrane’s resting potential in the brain.</abstract><cop>New York</cop><pub>Humana Press Inc</pub><pmid>21710140</pmid><doi>10.1007/s12035-011-8194-0</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Action Potentials - physiology Animals Antibody Specificity Biomedical and Life Sciences Biomedicine Cell Biology Cell membranes Cells, Cultured Cercopithecus aethiops COS Cells Cullin Cullin Proteins - metabolism Epilepsy Excitability Gene Expression Regulation Genes Hippocampus Hippocampus - metabolism Hippocampus - pathology Homology Humans Immunoprecipitation Ion Channel Gating - genetics Membrane potential Mice Myoclonic Epilepsies, Progressive - genetics Neurobiology Neurology Neurons Neurons - metabolism Neurons - pathology Neurosciences Nonsense mutation Olfactory Bulb - metabolism Olfactory Bulb - pathology Phenotypes Potassium Potassium Channels - genetics Potassium Channels - metabolism Potassium conductance Poxvirus Protein Binding Protein Multimerization Protein Transport Purkinje cells Purkinje Cells - metabolism Purkinje Cells - pathology RNA, Messenger - genetics RNA, Messenger - metabolism Zinc finger proteins |
title | Progressive Myoclonic Epilepsy-Associated Gene KCTD7 is a Regulator of Potassium Conductance in Neurons |
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