Unexpected phenotypic effects of a transgene integration causing a knockout of the endogenous Contactin-5 gene in mice
Contactins (Cntn1-6) are a family of neuronal membrane proteins expressed in the brain. They are required for establishing cell-to-cell contacts between neurons and for the growth and maturation of the axons. In humans, structural genomic variations in the Contactin genes are implicated in neurodeve...
Gespeichert in:
| Veröffentlicht in: | Transgenic research 2018-02, Vol.27 (1), p.1-13 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 13 |
|---|---|
| container_issue | 1 |
| container_start_page | 1 |
| container_title | Transgenic research |
| container_volume | 27 |
| creator | Smirnov, Alexander V. Kontsevaya, Galina V. Feofanova, Natalia A. Anisimova, Margarita V. Serova, Irina A. Gerlinskaya, Lyudmila A. Battulin, Nariman R. Moshkin, Mikhail P. Serov, Oleg L. |
| description | Contactins (Cntn1-6) are a family of neuronal membrane proteins expressed in the brain. They are required for establishing cell-to-cell contacts between neurons and for the growth and maturation of the axons. In humans, structural genomic variations in the Contactin genes are implicated in neurodevelopmental disorders. In addition, population genetic studies associate Contactins loci with obesity and hypertension. Cntn5 knockout mice were first described in 2003, but showed no gross physiological or behavioral abnormalities (just minor auditory defects). We report a novel Cntn5 knockout mouse line generated by a random transgene integration as an outcome of pronuclear microinjection. Investigation of the transgene integration site revealed that the 6Kbp transgene construct coding for the human granulocyte–macrophage colony-stimulating factor (hGMCSF) replaced 170 Kbp of the Cntn5 gene, including four exons. Reverse transcription PCR analysis of the Cntn5 transcripts in the wild-type and transgenic mouse lines showed that splicing of the transgene leads to a set of chimeric hGMCSF-Cntn5 transcript variants, none of which encode functional Cntn5 protein due to introduction of stop codons. Although Cntn5 knockout animals displayed no abnormalities in behavior, we noted that they were leaner, with less body mass and fat percentage than wild-type animals. Their cardiovascular parameters (heart rate, blood pressure and blood flow speed) were elevated compared to controls. These findings link Cntn5 deficiency to obesity and hypertension. |
| doi_str_mv | 10.1007/s11248-017-0053-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1979499999</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1979499999</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-cb14ee567d2b9bc62ea1c9768ad1f215c44508e6ad2debd7797bb129928bfe1c3</originalsourceid><addsrcrecordid>eNp1kUtrGzEURkVpiJ3HD-imCLrpRomkmdFjWUyaBALdNGuh0dyxxw9pKmlK_O8jx24pgWoj0D3fpwsHoU-M3jBK5W1ijNeKUCYJpU1F9h_QnDWyIroS6iOaUy04UYrpGbpIaU1pSanqHM245qIWUs_R72cPLyO4DB0eV-BD3o-Dw9D35S3h0GOLc7Q-LcEDHnyGZbR5CB47O6XBL8t844PbhCkf6LwCDL4LBQ9Twovgs3V58KTBpwa8GxxcobPebhNcn-5L9Pz97ufigTz9uH9cfHsirpI8E9eyGqARsuOtbp3gYJnTUijbsZ6zxtV1QxUI2_EO2k5KLduWca25antgrrpEX4-9Ywy_JkjZ7IbkYLu1Hsp-hmmpa304Bf3yDl2HKfqy3RtFRaVkUyh2pFwMKUXozRiHnY17w6g5SDFHKaZIMQcpZl8yn0_NU7uD7m_ij4UC8COQysgvIf7z9X9bXwHUBpmH</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1979063875</pqid></control><display><type>article</type><title>Unexpected phenotypic effects of a transgene integration causing a knockout of the endogenous Contactin-5 gene in mice</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Smirnov, Alexander V. ; Kontsevaya, Galina V. ; Feofanova, Natalia A. ; Anisimova, Margarita V. ; Serova, Irina A. ; Gerlinskaya, Lyudmila A. ; Battulin, Nariman R. ; Moshkin, Mikhail P. ; Serov, Oleg L.</creator><creatorcontrib>Smirnov, Alexander V. ; Kontsevaya, Galina V. ; Feofanova, Natalia A. ; Anisimova, Margarita V. ; Serova, Irina A. ; Gerlinskaya, Lyudmila A. ; Battulin, Nariman R. ; Moshkin, Mikhail P. ; Serov, Oleg L.</creatorcontrib><description>Contactins (Cntn1-6) are a family of neuronal membrane proteins expressed in the brain. They are required for establishing cell-to-cell contacts between neurons and for the growth and maturation of the axons. In humans, structural genomic variations in the Contactin genes are implicated in neurodevelopmental disorders. In addition, population genetic studies associate Contactins loci with obesity and hypertension. Cntn5 knockout mice were first described in 2003, but showed no gross physiological or behavioral abnormalities (just minor auditory defects). We report a novel Cntn5 knockout mouse line generated by a random transgene integration as an outcome of pronuclear microinjection. Investigation of the transgene integration site revealed that the 6Kbp transgene construct coding for the human granulocyte–macrophage colony-stimulating factor (hGMCSF) replaced 170 Kbp of the Cntn5 gene, including four exons. Reverse transcription PCR analysis of the Cntn5 transcripts in the wild-type and transgenic mouse lines showed that splicing of the transgene leads to a set of chimeric hGMCSF-Cntn5 transcript variants, none of which encode functional Cntn5 protein due to introduction of stop codons. Although Cntn5 knockout animals displayed no abnormalities in behavior, we noted that they were leaner, with less body mass and fat percentage than wild-type animals. Their cardiovascular parameters (heart rate, blood pressure and blood flow speed) were elevated compared to controls. These findings link Cntn5 deficiency to obesity and hypertension.</description><identifier>ISSN: 0962-8819</identifier><identifier>EISSN: 1573-9368</identifier><identifier>DOI: 10.1007/s11248-017-0053-y</identifier><identifier>PMID: 29264679</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Animal Genetics and Genomics ; Animals ; Auditory defects ; Axons ; Biomedical and Life Sciences ; Biomedical Engineering/Biotechnology ; Blood flow ; Blood pressure ; Body Composition - genetics ; Body Composition - physiology ; Body mass ; CNTN5 gene ; Coding ; Codons ; Colony-stimulating factor ; Contactin ; Contactins - genetics ; Drinking - genetics ; Eating - genetics ; Exons ; Female ; Gene Expression Regulation ; Genetic Engineering ; Granulocyte-macrophage colony-stimulating factor ; Granulocyte-Macrophage Colony-Stimulating Factor - genetics ; Heart rate ; Humans ; Hypertension ; Hypertension - genetics ; Integration ; Life Sciences ; Macrophages ; Male ; Membrane proteins ; Mice ; Mice, Knockout ; Mice, Transgenic - genetics ; Microinjection ; Molecular Medicine ; Neurodevelopmental disorders ; Obesity ; Original Paper ; Phenotype ; Plant Genetics and Genomics ; Polymerase Chain Reaction ; Population genetics ; Population studies ; Proteins ; Reverse transcription ; Rodents ; Splicing ; Transgenes ; Transgenic mice ; Transgenics</subject><ispartof>Transgenic research, 2018-02, Vol.27 (1), p.1-13</ispartof><rights>Springer International Publishing AG, part of Springer Nature 2017</rights><rights>Transgenic Research is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-cb14ee567d2b9bc62ea1c9768ad1f215c44508e6ad2debd7797bb129928bfe1c3</citedby><cites>FETCH-LOGICAL-c372t-cb14ee567d2b9bc62ea1c9768ad1f215c44508e6ad2debd7797bb129928bfe1c3</cites><orcidid>0000-0001-5152-9914</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/s11248-017-0053-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11248-017-0053-y$$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/29264679$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Smirnov, Alexander V.</creatorcontrib><creatorcontrib>Kontsevaya, Galina V.</creatorcontrib><creatorcontrib>Feofanova, Natalia A.</creatorcontrib><creatorcontrib>Anisimova, Margarita V.</creatorcontrib><creatorcontrib>Serova, Irina A.</creatorcontrib><creatorcontrib>Gerlinskaya, Lyudmila A.</creatorcontrib><creatorcontrib>Battulin, Nariman R.</creatorcontrib><creatorcontrib>Moshkin, Mikhail P.</creatorcontrib><creatorcontrib>Serov, Oleg L.</creatorcontrib><title>Unexpected phenotypic effects of a transgene integration causing a knockout of the endogenous Contactin-5 gene in mice</title><title>Transgenic research</title><addtitle>Transgenic Res</addtitle><addtitle>Transgenic Res</addtitle><description>Contactins (Cntn1-6) are a family of neuronal membrane proteins expressed in the brain. They are required for establishing cell-to-cell contacts between neurons and for the growth and maturation of the axons. In humans, structural genomic variations in the Contactin genes are implicated in neurodevelopmental disorders. In addition, population genetic studies associate Contactins loci with obesity and hypertension. Cntn5 knockout mice were first described in 2003, but showed no gross physiological or behavioral abnormalities (just minor auditory defects). We report a novel Cntn5 knockout mouse line generated by a random transgene integration as an outcome of pronuclear microinjection. Investigation of the transgene integration site revealed that the 6Kbp transgene construct coding for the human granulocyte–macrophage colony-stimulating factor (hGMCSF) replaced 170 Kbp of the Cntn5 gene, including four exons. Reverse transcription PCR analysis of the Cntn5 transcripts in the wild-type and transgenic mouse lines showed that splicing of the transgene leads to a set of chimeric hGMCSF-Cntn5 transcript variants, none of which encode functional Cntn5 protein due to introduction of stop codons. Although Cntn5 knockout animals displayed no abnormalities in behavior, we noted that they were leaner, with less body mass and fat percentage than wild-type animals. Their cardiovascular parameters (heart rate, blood pressure and blood flow speed) were elevated compared to controls. These findings link Cntn5 deficiency to obesity and hypertension.</description><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>Auditory defects</subject><subject>Axons</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedical Engineering/Biotechnology</subject><subject>Blood flow</subject><subject>Blood pressure</subject><subject>Body Composition - genetics</subject><subject>Body Composition - physiology</subject><subject>Body mass</subject><subject>CNTN5 gene</subject><subject>Coding</subject><subject>Codons</subject><subject>Colony-stimulating factor</subject><subject>Contactin</subject><subject>Contactins - genetics</subject><subject>Drinking - genetics</subject><subject>Eating - genetics</subject><subject>Exons</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Genetic Engineering</subject><subject>Granulocyte-macrophage colony-stimulating factor</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - genetics</subject><subject>Heart rate</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension - genetics</subject><subject>Integration</subject><subject>Life Sciences</subject><subject>Macrophages</subject><subject>Male</subject><subject>Membrane proteins</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic - genetics</subject><subject>Microinjection</subject><subject>Molecular Medicine</subject><subject>Neurodevelopmental disorders</subject><subject>Obesity</subject><subject>Original Paper</subject><subject>Phenotype</subject><subject>Plant Genetics and Genomics</subject><subject>Polymerase Chain Reaction</subject><subject>Population genetics</subject><subject>Population studies</subject><subject>Proteins</subject><subject>Reverse transcription</subject><subject>Rodents</subject><subject>Splicing</subject><subject>Transgenes</subject><subject>Transgenic mice</subject><subject>Transgenics</subject><issn>0962-8819</issn><issn>1573-9368</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</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>eNp1kUtrGzEURkVpiJ3HD-imCLrpRomkmdFjWUyaBALdNGuh0dyxxw9pKmlK_O8jx24pgWoj0D3fpwsHoU-M3jBK5W1ijNeKUCYJpU1F9h_QnDWyIroS6iOaUy04UYrpGbpIaU1pSanqHM245qIWUs_R72cPLyO4DB0eV-BD3o-Dw9D35S3h0GOLc7Q-LcEDHnyGZbR5CB47O6XBL8t844PbhCkf6LwCDL4LBQ9Twovgs3V58KTBpwa8GxxcobPebhNcn-5L9Pz97ufigTz9uH9cfHsirpI8E9eyGqARsuOtbp3gYJnTUijbsZ6zxtV1QxUI2_EO2k5KLduWca25antgrrpEX4-9Ywy_JkjZ7IbkYLu1Hsp-hmmpa304Bf3yDl2HKfqy3RtFRaVkUyh2pFwMKUXozRiHnY17w6g5SDFHKaZIMQcpZl8yn0_NU7uD7m_ij4UC8COQysgvIf7z9X9bXwHUBpmH</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Smirnov, Alexander V.</creator><creator>Kontsevaya, Galina V.</creator><creator>Feofanova, Natalia A.</creator><creator>Anisimova, Margarita V.</creator><creator>Serova, Irina A.</creator><creator>Gerlinskaya, Lyudmila A.</creator><creator>Battulin, Nariman R.</creator><creator>Moshkin, Mikhail P.</creator><creator>Serov, Oleg L.</creator><general>Springer International Publishing</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>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</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>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5152-9914</orcidid></search><sort><creationdate>20180201</creationdate><title>Unexpected phenotypic effects of a transgene integration causing a knockout of the endogenous Contactin-5 gene in mice</title><author>Smirnov, Alexander V. ; Kontsevaya, Galina V. ; Feofanova, Natalia A. ; Anisimova, Margarita V. ; Serova, Irina A. ; Gerlinskaya, Lyudmila A. ; Battulin, Nariman R. ; Moshkin, Mikhail P. ; Serov, Oleg L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-cb14ee567d2b9bc62ea1c9768ad1f215c44508e6ad2debd7797bb129928bfe1c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animal Genetics and Genomics</topic><topic>Animals</topic><topic>Auditory defects</topic><topic>Axons</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedical Engineering/Biotechnology</topic><topic>Blood flow</topic><topic>Blood pressure</topic><topic>Body Composition - genetics</topic><topic>Body Composition - physiology</topic><topic>Body mass</topic><topic>CNTN5 gene</topic><topic>Coding</topic><topic>Codons</topic><topic>Colony-stimulating factor</topic><topic>Contactin</topic><topic>Contactins - genetics</topic><topic>Drinking - genetics</topic><topic>Eating - genetics</topic><topic>Exons</topic><topic>Female</topic><topic>Gene Expression Regulation</topic><topic>Genetic Engineering</topic><topic>Granulocyte-macrophage colony-stimulating factor</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - genetics</topic><topic>Heart rate</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension - genetics</topic><topic>Integration</topic><topic>Life Sciences</topic><topic>Macrophages</topic><topic>Male</topic><topic>Membrane proteins</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mice, Transgenic - genetics</topic><topic>Microinjection</topic><topic>Molecular Medicine</topic><topic>Neurodevelopmental disorders</topic><topic>Obesity</topic><topic>Original Paper</topic><topic>Phenotype</topic><topic>Plant Genetics and Genomics</topic><topic>Polymerase Chain Reaction</topic><topic>Population genetics</topic><topic>Population studies</topic><topic>Proteins</topic><topic>Reverse transcription</topic><topic>Rodents</topic><topic>Splicing</topic><topic>Transgenes</topic><topic>Transgenic mice</topic><topic>Transgenics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Smirnov, Alexander V.</creatorcontrib><creatorcontrib>Kontsevaya, Galina V.</creatorcontrib><creatorcontrib>Feofanova, Natalia A.</creatorcontrib><creatorcontrib>Anisimova, Margarita V.</creatorcontrib><creatorcontrib>Serova, Irina A.</creatorcontrib><creatorcontrib>Gerlinskaya, Lyudmila A.</creatorcontrib><creatorcontrib>Battulin, Nariman R.</creatorcontrib><creatorcontrib>Moshkin, Mikhail P.</creatorcontrib><creatorcontrib>Serov, Oleg L.</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>Neurosciences Abstracts</collection><collection>Nucleic Acids 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>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>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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Transgenic research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Smirnov, Alexander V.</au><au>Kontsevaya, Galina V.</au><au>Feofanova, Natalia A.</au><au>Anisimova, Margarita V.</au><au>Serova, Irina A.</au><au>Gerlinskaya, Lyudmila A.</au><au>Battulin, Nariman R.</au><au>Moshkin, Mikhail P.</au><au>Serov, Oleg L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Unexpected phenotypic effects of a transgene integration causing a knockout of the endogenous Contactin-5 gene in mice</atitle><jtitle>Transgenic research</jtitle><stitle>Transgenic Res</stitle><addtitle>Transgenic Res</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>27</volume><issue>1</issue><spage>1</spage><epage>13</epage><pages>1-13</pages><issn>0962-8819</issn><eissn>1573-9368</eissn><abstract>Contactins (Cntn1-6) are a family of neuronal membrane proteins expressed in the brain. They are required for establishing cell-to-cell contacts between neurons and for the growth and maturation of the axons. In humans, structural genomic variations in the Contactin genes are implicated in neurodevelopmental disorders. In addition, population genetic studies associate Contactins loci with obesity and hypertension. Cntn5 knockout mice were first described in 2003, but showed no gross physiological or behavioral abnormalities (just minor auditory defects). We report a novel Cntn5 knockout mouse line generated by a random transgene integration as an outcome of pronuclear microinjection. Investigation of the transgene integration site revealed that the 6Kbp transgene construct coding for the human granulocyte–macrophage colony-stimulating factor (hGMCSF) replaced 170 Kbp of the Cntn5 gene, including four exons. Reverse transcription PCR analysis of the Cntn5 transcripts in the wild-type and transgenic mouse lines showed that splicing of the transgene leads to a set of chimeric hGMCSF-Cntn5 transcript variants, none of which encode functional Cntn5 protein due to introduction of stop codons. Although Cntn5 knockout animals displayed no abnormalities in behavior, we noted that they were leaner, with less body mass and fat percentage than wild-type animals. Their cardiovascular parameters (heart rate, blood pressure and blood flow speed) were elevated compared to controls. These findings link Cntn5 deficiency to obesity and hypertension.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>29264679</pmid><doi>10.1007/s11248-017-0053-y</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-5152-9914</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0962-8819 |
| ispartof | Transgenic research, 2018-02, Vol.27 (1), p.1-13 |
| issn | 0962-8819 1573-9368 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1979499999 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animal Genetics and Genomics Animals Auditory defects Axons Biomedical and Life Sciences Biomedical Engineering/Biotechnology Blood flow Blood pressure Body Composition - genetics Body Composition - physiology Body mass CNTN5 gene Coding Codons Colony-stimulating factor Contactin Contactins - genetics Drinking - genetics Eating - genetics Exons Female Gene Expression Regulation Genetic Engineering Granulocyte-macrophage colony-stimulating factor Granulocyte-Macrophage Colony-Stimulating Factor - genetics Heart rate Humans Hypertension Hypertension - genetics Integration Life Sciences Macrophages Male Membrane proteins Mice Mice, Knockout Mice, Transgenic - genetics Microinjection Molecular Medicine Neurodevelopmental disorders Obesity Original Paper Phenotype Plant Genetics and Genomics Polymerase Chain Reaction Population genetics Population studies Proteins Reverse transcription Rodents Splicing Transgenes Transgenic mice Transgenics |
| title | Unexpected phenotypic effects of a transgene integration causing a knockout of the endogenous Contactin-5 gene in mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-20T06%3A45%3A16IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Unexpected%20phenotypic%20effects%20of%20a%20transgene%20integration%20causing%20a%20knockout%20of%20the%20endogenous%20Contactin-5%20gene%20in%20mice&rft.jtitle=Transgenic%20research&rft.au=Smirnov,%20Alexander%20V.&rft.date=2018-02-01&rft.volume=27&rft.issue=1&rft.spage=1&rft.epage=13&rft.pages=1-13&rft.issn=0962-8819&rft.eissn=1573-9368&rft_id=info:doi/10.1007/s11248-017-0053-y&rft_dat=%3Cproquest_cross%3E1979499999%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1979063875&rft_id=info:pmid/29264679&rfr_iscdi=true |