Generation and characterization of the Anp32e-deficient mouse
Accumulated literature suggests that the acidic nuclear phosphoprotein 32 kilodalton (Anp32) proteins control multiple cellular activities through different molecular mechanisms. Like other Anp32 family members, Anp32e (a.k.a. Cpd1, PhapIII) has been conserved throughout vertebrate evolution, sugges...
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| creator | Reilly, Patrick T Afzal, Samia Wakeham, Andrew Haight, Jillian You-Ten, Annick Zaugg, Kathrin Dembowy, Joanna Young, Ashley Mak, Tak W |
| description | Accumulated literature suggests that the acidic nuclear phosphoprotein 32 kilodalton (Anp32) proteins control multiple cellular activities through different molecular mechanisms. Like other Anp32 family members, Anp32e (a.k.a. Cpd1, PhapIII) has been conserved throughout vertebrate evolution, suggesting that it has an important function in organismal survival.
Here, we demonstrate that the Anp32e gene can be deleted in mice without any apparent effect on their wellbeing. No defects in thymocyte apoptosis in response to various stresses, fibroblast growth, gross behaviour, physical ability, or pathogenesis were defined. Furthermore, combined deletion of Anp32a and Anp32e also resulted in a viable and apparently healthy mouse.
These results provide evidence that significant functional redundancy exists among Anp32 family members. |
| doi_str_mv | 10.1371/journal.pone.0013597 |
| format | Article |
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Here, we demonstrate that the Anp32e gene can be deleted in mice without any apparent effect on their wellbeing. No defects in thymocyte apoptosis in response to various stresses, fibroblast growth, gross behaviour, physical ability, or pathogenesis were defined. Furthermore, combined deletion of Anp32a and Anp32e also resulted in a viable and apparently healthy mouse.
These results provide evidence that significant functional redundancy exists among Anp32 family members.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0013597</identifier><identifier>PMID: 21049064</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Apoptosis ; Brain research ; Cell Cycle Proteins - genetics ; Cell growth ; Clonal deletion ; Cloning ; Cytochrome ; Defects ; Deoxyribonucleic acid ; Developmental Biology/Neurodevelopment ; DNA ; Drosophila ; Gastric cancer ; Gene expression ; Genetics and Genomics/Cancer Genetics ; Genetics and Genomics/Disease Models ; Genomes ; Health care networks ; Insects ; Lymphoma ; Medical research ; Mice ; Mice, Inbred C57BL ; Molecular modelling ; Multiple myeloma ; Mutation ; Nerve Tissue Proteins - genetics ; Nuclear Proteins - genetics ; Pathogenesis ; Phosphatase ; Physiology ; Proteins ; Redundancy ; Reverse Transcriptase Polymerase Chain Reaction ; Rodents ; Stomach cancer ; Studies</subject><ispartof>PloS one, 2010-10, Vol.5 (10), p.e13597-e13597</ispartof><rights>COPYRIGHT 2010 Public Library of Science</rights><rights>2010 Reilly et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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>Reilly et al. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c757t-e900cefe4e82cb65e3bd02bf65e5491c91234b0f92e397d1ead9606baca03ddc3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2964292/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2964292/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21049064$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reilly, Patrick T</creatorcontrib><creatorcontrib>Afzal, Samia</creatorcontrib><creatorcontrib>Wakeham, Andrew</creatorcontrib><creatorcontrib>Haight, Jillian</creatorcontrib><creatorcontrib>You-Ten, Annick</creatorcontrib><creatorcontrib>Zaugg, Kathrin</creatorcontrib><creatorcontrib>Dembowy, Joanna</creatorcontrib><creatorcontrib>Young, Ashley</creatorcontrib><creatorcontrib>Mak, Tak W</creatorcontrib><title>Generation and characterization of the Anp32e-deficient mouse</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Accumulated literature suggests that the acidic nuclear phosphoprotein 32 kilodalton (Anp32) proteins control multiple cellular activities through different molecular mechanisms. Like other Anp32 family members, Anp32e (a.k.a. Cpd1, PhapIII) has been conserved throughout vertebrate evolution, suggesting that it has an important function in organismal survival.
Here, we demonstrate that the Anp32e gene can be deleted in mice without any apparent effect on their wellbeing. No defects in thymocyte apoptosis in response to various stresses, fibroblast growth, gross behaviour, physical ability, or pathogenesis were defined. Furthermore, combined deletion of Anp32a and Anp32e also resulted in a viable and apparently healthy mouse.
These results provide evidence that significant functional redundancy exists among Anp32 family members.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Brain research</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell growth</subject><subject>Clonal deletion</subject><subject>Cloning</subject><subject>Cytochrome</subject><subject>Defects</subject><subject>Deoxyribonucleic acid</subject><subject>Developmental Biology/Neurodevelopment</subject><subject>DNA</subject><subject>Drosophila</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Genetics and Genomics/Cancer Genetics</subject><subject>Genetics and Genomics/Disease Models</subject><subject>Genomes</subject><subject>Health care networks</subject><subject>Insects</subject><subject>Lymphoma</subject><subject>Medical research</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular modelling</subject><subject>Multiple myeloma</subject><subject>Mutation</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nuclear Proteins - genetics</subject><subject>Pathogenesis</subject><subject>Phosphatase</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Redundancy</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Rodents</subject><subject>Stomach cancer</subject><subject>Studies</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7jr6D0QLguLFjPlq2lwoDIuuAwsLft2GNDmZydA2Y9KK-utNne4ylb2QXCScPOc9OSdvlj3FaIVpid_s_RA61awOvoMVQpgWoryXnWNByZITRO-fnM-yRzHuESpoxfnD7IxgxATi7Dx7ewkdBNU73-WqM7neqaB0D8H9Pga9zfsd5OvuQAksDVinHXR93vohwuPsgVVNhCfTvsi-fnj_5eLj8ur6cnOxvlrqsij7JQiENFhgUBFd8wJobRCpbToVTGAtMKGsRlYQoKI0GJQRHPFaaYWoMZousudH3UPjo5w6jxITQSjCpCKJ2BwJ49VeHoJrVfglvXLyb8CHrVShd7oBWaCqZNpiXmHDDOa1YVWqUlpccMpZkbTeTdWGugWjU7tBNTPR-U3ndnLrf0giOBuftMheTQLBfx8g9rJ1UUPTqA7S2GTJCSsJEWOpF_-Qdzc3UVuV3u8661NZPWrKNStpxTDlIlGrO6i0DLROJ5dYl-KzhNezhMT08LPfqiFGufn86f_Z629z9uUJuwPV9Lvom2H0U5yD7Ajq4GMMYG9njJEcTX4zDTmaXE4mT2nPTv_nNunG1fQPKSL1sg</recordid><startdate>20101026</startdate><enddate>20101026</enddate><creator>Reilly, Patrick T</creator><creator>Afzal, Samia</creator><creator>Wakeham, Andrew</creator><creator>Haight, Jillian</creator><creator>You-Ten, Annick</creator><creator>Zaugg, Kathrin</creator><creator>Dembowy, Joanna</creator><creator>Young, Ashley</creator><creator>Mak, Tak W</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>IOV</scope><scope>ISR</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>AEUYN</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>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20101026</creationdate><title>Generation and characterization of the Anp32e-deficient mouse</title><author>Reilly, Patrick T ; Afzal, Samia ; Wakeham, Andrew ; Haight, Jillian ; You-Ten, Annick ; Zaugg, Kathrin ; Dembowy, Joanna ; Young, Ashley ; Mak, Tak W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c757t-e900cefe4e82cb65e3bd02bf65e5491c91234b0f92e397d1ead9606baca03ddc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Brain research</topic><topic>Cell Cycle Proteins - 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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>Reilly, Patrick T</au><au>Afzal, Samia</au><au>Wakeham, Andrew</au><au>Haight, Jillian</au><au>You-Ten, Annick</au><au>Zaugg, Kathrin</au><au>Dembowy, Joanna</au><au>Young, Ashley</au><au>Mak, Tak W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Generation and characterization of the Anp32e-deficient mouse</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2010-10-26</date><risdate>2010</risdate><volume>5</volume><issue>10</issue><spage>e13597</spage><epage>e13597</epage><pages>e13597-e13597</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Accumulated literature suggests that the acidic nuclear phosphoprotein 32 kilodalton (Anp32) proteins control multiple cellular activities through different molecular mechanisms. Like other Anp32 family members, Anp32e (a.k.a. Cpd1, PhapIII) has been conserved throughout vertebrate evolution, suggesting that it has an important function in organismal survival.
Here, we demonstrate that the Anp32e gene can be deleted in mice without any apparent effect on their wellbeing. No defects in thymocyte apoptosis in response to various stresses, fibroblast growth, gross behaviour, physical ability, or pathogenesis were defined. Furthermore, combined deletion of Anp32a and Anp32e also resulted in a viable and apparently healthy mouse.
These results provide evidence that significant functional redundancy exists among Anp32 family members.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21049064</pmid><doi>10.1371/journal.pone.0013597</doi><tpages>e13597</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Brain research Cell Cycle Proteins - genetics Cell growth Clonal deletion Cloning Cytochrome Defects Deoxyribonucleic acid Developmental Biology/Neurodevelopment DNA Drosophila Gastric cancer Gene expression Genetics and Genomics/Cancer Genetics Genetics and Genomics/Disease Models Genomes Health care networks Insects Lymphoma Medical research Mice Mice, Inbred C57BL Molecular modelling Multiple myeloma Mutation Nerve Tissue Proteins - genetics Nuclear Proteins - genetics Pathogenesis Phosphatase Physiology Proteins Redundancy Reverse Transcriptase Polymerase Chain Reaction Rodents Stomach cancer Studies |
| title | Generation and characterization of the Anp32e-deficient mouse |
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