Gene expression and pathway analysis of effects of the CMAH deactivation on mouse lung, kidney and heart
N-glycolylneuraminic acid (Neu5Gc) is generated by hydroxylation of CMP-Neu5Ac to CMP-Neu5Gc, catalyzed by CMP-Neu5Ac hydroxylase (CMAH). However, humans lack this common mammalian cell surface molecule, Neu5Gc, due to inactivation of the CMAH gene during evolution. CMAH is one of several human-spec...
Gespeichert in:
| Veröffentlicht in: | PloS one 2014-09, Vol.9 (9), p.e107559-e107559 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e107559 |
|---|---|
| container_issue | 9 |
| container_start_page | e107559 |
| container_title | PloS one |
| container_volume | 9 |
| creator | Kwon, Deug-Nam Chang, Byung-Soo Kim, Jin-Hoi |
| description | N-glycolylneuraminic acid (Neu5Gc) is generated by hydroxylation of CMP-Neu5Ac to CMP-Neu5Gc, catalyzed by CMP-Neu5Ac hydroxylase (CMAH). However, humans lack this common mammalian cell surface molecule, Neu5Gc, due to inactivation of the CMAH gene during evolution. CMAH is one of several human-specific genes whose function has been lost by disruption or deletion of the coding frame. It has been suggested that CMAH inactivation has resulted in biochemical or physiological characteristics that have resulted in human-specific diseases.
To identify differential gene expression profiles associated with the loss of Neu5Gc expression, we performed microarray analysis using Illumina MouseRef-8 v2 Expression BeadChip, using the main tissues (lung, kidney, and heart) from control mice and CMP-Neu5Ac hydroxylase (Cmah) gene knock-out mice, respectively. Out of a total of 25,697 genes, 204, 162, and 147 genes were found to be significantly modulated in the lung, kidney, and heart tissues of the Cmah null mouse, respectively. In this study, we examined the gene expression profiles, using three commercial pathway analysis software packages: Ingenuity Pathways Analysis, Kyoto Encyclopedia of Genes and Genomes analysis, and Pathway Studio. The gene ontology analysis revealed that the top 6 biological processes of these genes included protein metabolism and modification, signal transduction, lipid, fatty acid, and steroid metabolism, nucleoside, nucleotide and nucleic acid metabolism, immunity and defense, and carbohydrate metabolism. Gene interaction network analysis showed a common network that was common to the different tissues of the Cmah null mouse. However, the expression of most sialytransferase mRNAs of Hanganutziu-Deicher antigen, sialy-Tn antigen, Forssman antigen, and Tn antigen was significantly down-regulated in the liver tissue of Cmah null mice.
Mice bearing a human-like deletion of the Cmah gene serve as an important model for the study of abnormal pathogenesis and/or metabolism caused by the evolutionary loss of Neu5Gc synthesis in humans. |
| doi_str_mv | 10.1371/journal.pone.0107559 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_plos_</sourceid><recordid>TN_cdi_plos_journals_1562653751</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_c13cf11048164158bc461745ec86dba2</doaj_id><sourcerecordid>1563986399</sourcerecordid><originalsourceid>FETCH-LOGICAL-c526t-fb9ebbf8f92616eec0514055402ebc3a73bd6eae474ea5410c2931b143751bc3</originalsourceid><addsrcrecordid>eNptUk1v1DAUjBCIfsA_QBCJSw_s4ufP5IJUraCtVMSld8txXjZZsvZiJ4X99zi7adUiJFse2TPj954my94BWQJT8Hnjx-BMv9x5h0sCRAlRvshOoWR0ISlhL5_gk-wsxg0hghVSvs5OqKC0VEqdZu0VOszxzy5gjJ13uXF1vjND-9vsEzb9PnYx902OTYN2OMChxXz1_fI6r9HYobs3wyRMa-vHiHk_uvWn_GdXO9wf7Fo0YXiTvWpMH_HtfJ5nd9--3q2uF7c_rm5Wl7cLK6gcFk1VYlU1RVNSCRLREgGcCMEJxcoyo1hVSzTIFUcjOBBLSwYVcKYEJMJ59uFou-t91POMogYhqRQTJzFujozam43ehW5rwl570-nDhQ9rncrtbI_aArMNAOEFSA6iqCyXoLhAW8i6MjR5fZl_G6st1hbdEEz_zPT5i-tavfb3moNUZSmTwcVsEPyvEeOgt1202PfGYRrmVDcri7TLRP34D_X_3fEjywYfY8DmsRggesrNg0pPudFzbpLs_dNGHkUPQWF_AafywSI</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1562653751</pqid></control><display><type>article</type><title>Gene expression and pathway analysis of effects of the CMAH deactivation on mouse lung, kidney and heart</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Kwon, Deug-Nam ; Chang, Byung-Soo ; Kim, Jin-Hoi</creator><contributor>Sun, Qing-Yuan</contributor><creatorcontrib>Kwon, Deug-Nam ; Chang, Byung-Soo ; Kim, Jin-Hoi ; Sun, Qing-Yuan</creatorcontrib><description>N-glycolylneuraminic acid (Neu5Gc) is generated by hydroxylation of CMP-Neu5Ac to CMP-Neu5Gc, catalyzed by CMP-Neu5Ac hydroxylase (CMAH). However, humans lack this common mammalian cell surface molecule, Neu5Gc, due to inactivation of the CMAH gene during evolution. CMAH is one of several human-specific genes whose function has been lost by disruption or deletion of the coding frame. It has been suggested that CMAH inactivation has resulted in biochemical or physiological characteristics that have resulted in human-specific diseases.
To identify differential gene expression profiles associated with the loss of Neu5Gc expression, we performed microarray analysis using Illumina MouseRef-8 v2 Expression BeadChip, using the main tissues (lung, kidney, and heart) from control mice and CMP-Neu5Ac hydroxylase (Cmah) gene knock-out mice, respectively. Out of a total of 25,697 genes, 204, 162, and 147 genes were found to be significantly modulated in the lung, kidney, and heart tissues of the Cmah null mouse, respectively. In this study, we examined the gene expression profiles, using three commercial pathway analysis software packages: Ingenuity Pathways Analysis, Kyoto Encyclopedia of Genes and Genomes analysis, and Pathway Studio. The gene ontology analysis revealed that the top 6 biological processes of these genes included protein metabolism and modification, signal transduction, lipid, fatty acid, and steroid metabolism, nucleoside, nucleotide and nucleic acid metabolism, immunity and defense, and carbohydrate metabolism. Gene interaction network analysis showed a common network that was common to the different tissues of the Cmah null mouse. However, the expression of most sialytransferase mRNAs of Hanganutziu-Deicher antigen, sialy-Tn antigen, Forssman antigen, and Tn antigen was significantly down-regulated in the liver tissue of Cmah null mice.
Mice bearing a human-like deletion of the Cmah gene serve as an important model for the study of abnormal pathogenesis and/or metabolism caused by the evolutionary loss of Neu5Gc synthesis in humans.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0107559</identifier><identifier>PMID: 25229777</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animal tissues ; Animals ; Antigens ; Bioinformatics ; Biological activity ; Biological evolution ; Biology ; Biology and Life Sciences ; Carbohydrate metabolism ; Carbohydrates ; Cell surface ; Clonal deletion ; Deactivation ; DNA microarrays ; Encyclopedias ; Evolution ; Evolutionary genetics ; Fatty acids ; Forssman antigen ; Gene deletion ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Knockout Techniques ; Gene Ontology ; Gene Regulatory Networks ; Genes ; Genomes ; Genotype ; Heart ; Hogs ; Hydroxylase ; Hydroxylation ; Immune system ; Immunity ; Immunoglobulins ; Immunohistochemistry ; Inactivation ; Kidney - metabolism ; Kidneys ; Laboratories ; Liver ; Lung - metabolism ; Lungs ; Male ; Mammals ; Medical research ; Metabolism ; Mice ; Mice, Knockout ; Mixed Function Oxygenases - genetics ; Mixed Function Oxygenases - metabolism ; Myocardium - metabolism ; Network analysis ; Ontology ; Pathogenesis ; Physiology ; Protein Interaction Maps ; Protein metabolism ; Protein turnover ; Research and Analysis Methods ; Sialyltransferases - genetics ; Sialyltransferases - metabolism ; Signal processing ; Signal Transduction ; Software packages ; Transcriptome ; Transduction</subject><ispartof>PloS one, 2014-09, Vol.9 (9), p.e107559-e107559</ispartof><rights>2014 Kwon et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Kwon et al 2014 Kwon et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-fb9ebbf8f92616eec0514055402ebc3a73bd6eae474ea5410c2931b143751bc3</citedby><cites>FETCH-LOGICAL-c526t-fb9ebbf8f92616eec0514055402ebc3a73bd6eae474ea5410c2931b143751bc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4167996/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4167996/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23870,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25229777$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Sun, Qing-Yuan</contributor><creatorcontrib>Kwon, Deug-Nam</creatorcontrib><creatorcontrib>Chang, Byung-Soo</creatorcontrib><creatorcontrib>Kim, Jin-Hoi</creatorcontrib><title>Gene expression and pathway analysis of effects of the CMAH deactivation on mouse lung, kidney and heart</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>N-glycolylneuraminic acid (Neu5Gc) is generated by hydroxylation of CMP-Neu5Ac to CMP-Neu5Gc, catalyzed by CMP-Neu5Ac hydroxylase (CMAH). However, humans lack this common mammalian cell surface molecule, Neu5Gc, due to inactivation of the CMAH gene during evolution. CMAH is one of several human-specific genes whose function has been lost by disruption or deletion of the coding frame. It has been suggested that CMAH inactivation has resulted in biochemical or physiological characteristics that have resulted in human-specific diseases.
To identify differential gene expression profiles associated with the loss of Neu5Gc expression, we performed microarray analysis using Illumina MouseRef-8 v2 Expression BeadChip, using the main tissues (lung, kidney, and heart) from control mice and CMP-Neu5Ac hydroxylase (Cmah) gene knock-out mice, respectively. Out of a total of 25,697 genes, 204, 162, and 147 genes were found to be significantly modulated in the lung, kidney, and heart tissues of the Cmah null mouse, respectively. In this study, we examined the gene expression profiles, using three commercial pathway analysis software packages: Ingenuity Pathways Analysis, Kyoto Encyclopedia of Genes and Genomes analysis, and Pathway Studio. The gene ontology analysis revealed that the top 6 biological processes of these genes included protein metabolism and modification, signal transduction, lipid, fatty acid, and steroid metabolism, nucleoside, nucleotide and nucleic acid metabolism, immunity and defense, and carbohydrate metabolism. Gene interaction network analysis showed a common network that was common to the different tissues of the Cmah null mouse. However, the expression of most sialytransferase mRNAs of Hanganutziu-Deicher antigen, sialy-Tn antigen, Forssman antigen, and Tn antigen was significantly down-regulated in the liver tissue of Cmah null mice.
Mice bearing a human-like deletion of the Cmah gene serve as an important model for the study of abnormal pathogenesis and/or metabolism caused by the evolutionary loss of Neu5Gc synthesis in humans.</description><subject>Animal tissues</subject><subject>Animals</subject><subject>Antigens</subject><subject>Bioinformatics</subject><subject>Biological activity</subject><subject>Biological evolution</subject><subject>Biology</subject><subject>Biology and Life Sciences</subject><subject>Carbohydrate metabolism</subject><subject>Carbohydrates</subject><subject>Cell surface</subject><subject>Clonal deletion</subject><subject>Deactivation</subject><subject>DNA microarrays</subject><subject>Encyclopedias</subject><subject>Evolution</subject><subject>Evolutionary genetics</subject><subject>Fatty acids</subject><subject>Forssman antigen</subject><subject>Gene deletion</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Gene Knockout Techniques</subject><subject>Gene Ontology</subject><subject>Gene Regulatory Networks</subject><subject>Genes</subject><subject>Genomes</subject><subject>Genotype</subject><subject>Heart</subject><subject>Hogs</subject><subject>Hydroxylase</subject><subject>Hydroxylation</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Immunoglobulins</subject><subject>Immunohistochemistry</subject><subject>Inactivation</subject><subject>Kidney - metabolism</subject><subject>Kidneys</subject><subject>Laboratories</subject><subject>Liver</subject><subject>Lung - metabolism</subject><subject>Lungs</subject><subject>Male</subject><subject>Mammals</subject><subject>Medical research</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mixed Function Oxygenases - genetics</subject><subject>Mixed Function Oxygenases - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Network analysis</subject><subject>Ontology</subject><subject>Pathogenesis</subject><subject>Physiology</subject><subject>Protein Interaction Maps</subject><subject>Protein metabolism</subject><subject>Protein turnover</subject><subject>Research and Analysis Methods</subject><subject>Sialyltransferases - genetics</subject><subject>Sialyltransferases - metabolism</subject><subject>Signal processing</subject><subject>Signal Transduction</subject><subject>Software packages</subject><subject>Transcriptome</subject><subject>Transduction</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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><sourceid>DOA</sourceid><recordid>eNptUk1v1DAUjBCIfsA_QBCJSw_s4ufP5IJUraCtVMSld8txXjZZsvZiJ4X99zi7adUiJFse2TPj954my94BWQJT8Hnjx-BMv9x5h0sCRAlRvshOoWR0ISlhL5_gk-wsxg0hghVSvs5OqKC0VEqdZu0VOszxzy5gjJ13uXF1vjND-9vsEzb9PnYx902OTYN2OMChxXz1_fI6r9HYobs3wyRMa-vHiHk_uvWn_GdXO9wf7Fo0YXiTvWpMH_HtfJ5nd9--3q2uF7c_rm5Wl7cLK6gcFk1VYlU1RVNSCRLREgGcCMEJxcoyo1hVSzTIFUcjOBBLSwYVcKYEJMJ59uFou-t91POMogYhqRQTJzFujozam43ehW5rwl570-nDhQ9rncrtbI_aArMNAOEFSA6iqCyXoLhAW8i6MjR5fZl_G6st1hbdEEz_zPT5i-tavfb3moNUZSmTwcVsEPyvEeOgt1202PfGYRrmVDcri7TLRP34D_X_3fEjywYfY8DmsRggesrNg0pPudFzbpLs_dNGHkUPQWF_AafywSI</recordid><startdate>20140917</startdate><enddate>20140917</enddate><creator>Kwon, Deug-Nam</creator><creator>Chang, Byung-Soo</creator><creator>Kim, Jin-Hoi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140917</creationdate><title>Gene expression and pathway analysis of effects of the CMAH deactivation on mouse lung, kidney and heart</title><author>Kwon, Deug-Nam ; Chang, Byung-Soo ; Kim, Jin-Hoi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-fb9ebbf8f92616eec0514055402ebc3a73bd6eae474ea5410c2931b143751bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animal tissues</topic><topic>Animals</topic><topic>Antigens</topic><topic>Bioinformatics</topic><topic>Biological activity</topic><topic>Biological evolution</topic><topic>Biology</topic><topic>Biology and Life Sciences</topic><topic>Carbohydrate metabolism</topic><topic>Carbohydrates</topic><topic>Cell surface</topic><topic>Clonal deletion</topic><topic>Deactivation</topic><topic>DNA microarrays</topic><topic>Encyclopedias</topic><topic>Evolution</topic><topic>Evolutionary genetics</topic><topic>Fatty acids</topic><topic>Forssman antigen</topic><topic>Gene deletion</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Gene Knockout Techniques</topic><topic>Gene Ontology</topic><topic>Gene Regulatory Networks</topic><topic>Genes</topic><topic>Genomes</topic><topic>Genotype</topic><topic>Heart</topic><topic>Hogs</topic><topic>Hydroxylase</topic><topic>Hydroxylation</topic><topic>Immune system</topic><topic>Immunity</topic><topic>Immunoglobulins</topic><topic>Immunohistochemistry</topic><topic>Inactivation</topic><topic>Kidney - metabolism</topic><topic>Kidneys</topic><topic>Laboratories</topic><topic>Liver</topic><topic>Lung - metabolism</topic><topic>Lungs</topic><topic>Male</topic><topic>Mammals</topic><topic>Medical research</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mixed Function Oxygenases - genetics</topic><topic>Mixed Function Oxygenases - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Network analysis</topic><topic>Ontology</topic><topic>Pathogenesis</topic><topic>Physiology</topic><topic>Protein Interaction Maps</topic><topic>Protein metabolism</topic><topic>Protein turnover</topic><topic>Research and Analysis Methods</topic><topic>Sialyltransferases - genetics</topic><topic>Sialyltransferases - metabolism</topic><topic>Signal processing</topic><topic>Signal Transduction</topic><topic>Software packages</topic><topic>Transcriptome</topic><topic>Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kwon, Deug-Nam</creatorcontrib><creatorcontrib>Chang, Byung-Soo</creatorcontrib><creatorcontrib>Kim, Jin-Hoi</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kwon, Deug-Nam</au><au>Chang, Byung-Soo</au><au>Kim, Jin-Hoi</au><au>Sun, Qing-Yuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene expression and pathway analysis of effects of the CMAH deactivation on mouse lung, kidney and heart</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-09-17</date><risdate>2014</risdate><volume>9</volume><issue>9</issue><spage>e107559</spage><epage>e107559</epage><pages>e107559-e107559</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>N-glycolylneuraminic acid (Neu5Gc) is generated by hydroxylation of CMP-Neu5Ac to CMP-Neu5Gc, catalyzed by CMP-Neu5Ac hydroxylase (CMAH). However, humans lack this common mammalian cell surface molecule, Neu5Gc, due to inactivation of the CMAH gene during evolution. CMAH is one of several human-specific genes whose function has been lost by disruption or deletion of the coding frame. It has been suggested that CMAH inactivation has resulted in biochemical or physiological characteristics that have resulted in human-specific diseases.
To identify differential gene expression profiles associated with the loss of Neu5Gc expression, we performed microarray analysis using Illumina MouseRef-8 v2 Expression BeadChip, using the main tissues (lung, kidney, and heart) from control mice and CMP-Neu5Ac hydroxylase (Cmah) gene knock-out mice, respectively. Out of a total of 25,697 genes, 204, 162, and 147 genes were found to be significantly modulated in the lung, kidney, and heart tissues of the Cmah null mouse, respectively. In this study, we examined the gene expression profiles, using three commercial pathway analysis software packages: Ingenuity Pathways Analysis, Kyoto Encyclopedia of Genes and Genomes analysis, and Pathway Studio. The gene ontology analysis revealed that the top 6 biological processes of these genes included protein metabolism and modification, signal transduction, lipid, fatty acid, and steroid metabolism, nucleoside, nucleotide and nucleic acid metabolism, immunity and defense, and carbohydrate metabolism. Gene interaction network analysis showed a common network that was common to the different tissues of the Cmah null mouse. However, the expression of most sialytransferase mRNAs of Hanganutziu-Deicher antigen, sialy-Tn antigen, Forssman antigen, and Tn antigen was significantly down-regulated in the liver tissue of Cmah null mice.
Mice bearing a human-like deletion of the Cmah gene serve as an important model for the study of abnormal pathogenesis and/or metabolism caused by the evolutionary loss of Neu5Gc synthesis in humans.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25229777</pmid><doi>10.1371/journal.pone.0107559</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-09, Vol.9 (9), p.e107559-e107559 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1562653751 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animal tissues Animals Antigens Bioinformatics Biological activity Biological evolution Biology Biology and Life Sciences Carbohydrate metabolism Carbohydrates Cell surface Clonal deletion Deactivation DNA microarrays Encyclopedias Evolution Evolutionary genetics Fatty acids Forssman antigen Gene deletion Gene expression Gene Expression Profiling Gene Expression Regulation Gene Knockout Techniques Gene Ontology Gene Regulatory Networks Genes Genomes Genotype Heart Hogs Hydroxylase Hydroxylation Immune system Immunity Immunoglobulins Immunohistochemistry Inactivation Kidney - metabolism Kidneys Laboratories Liver Lung - metabolism Lungs Male Mammals Medical research Metabolism Mice Mice, Knockout Mixed Function Oxygenases - genetics Mixed Function Oxygenases - metabolism Myocardium - metabolism Network analysis Ontology Pathogenesis Physiology Protein Interaction Maps Protein metabolism Protein turnover Research and Analysis Methods Sialyltransferases - genetics Sialyltransferases - metabolism Signal processing Signal Transduction Software packages Transcriptome Transduction |
| title | Gene expression and pathway analysis of effects of the CMAH deactivation on mouse lung, kidney and heart |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-17T02%3A59%3A49IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Gene%20expression%20and%20pathway%20analysis%20of%20effects%20of%20the%20CMAH%20deactivation%20on%20mouse%20lung,%20kidney%20and%20heart&rft.jtitle=PloS%20one&rft.au=Kwon,%20Deug-Nam&rft.date=2014-09-17&rft.volume=9&rft.issue=9&rft.spage=e107559&rft.epage=e107559&rft.pages=e107559-e107559&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0107559&rft_dat=%3Cproquest_plos_%3E1563986399%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1562653751&rft_id=info:pmid/25229777&rft_doaj_id=oai_doaj_org_article_c13cf11048164158bc461745ec86dba2&rfr_iscdi=true |