Ectopic expression of systemic RNA interference defective protein in embryonic stem cells
RNA interference (RNAi), a post-transcriptional gene silencing mechanism originally described in Caenorhabditis elegans, involves sequence-specific mRNA degradation mediated by double-stranded RNAs (dsRNAs). Passive dsRNA uptake has been uniquely observed in C. elegans due to the expression of syste...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2007-06, Vol.357 (2), p.480-486 |
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| creator | Tsang, Suk Ying Moore, Jennifer C. Huizen, Rika Van Chan, Camie W.Y. Li, Ronald A. |
| description | RNA interference (RNAi), a post-transcriptional gene silencing mechanism originally described in
Caenorhabditis elegans, involves sequence-specific mRNA degradation mediated by double-stranded RNAs (dsRNAs). Passive dsRNA uptake has been uniquely observed in
C. elegans due to the expression of systemic RNA interference defective-1 (SID-1). Here we investigated the ability of ectopic SID-1 expression to enable passive cellular uptake of short interfering RNA (siRNA) or double stranded RNA (dsRNA) in pluripotent mouse embryonic stem cells (mESCs). When SID-1-GFP and the Firefly luciferase reporter gene (luc
Fir) were co-expressed in mESCs, luc
Fir activity could be suppressed by simple incubation with dsRNAs/siRNAs that were designed to specifically target luc
Fir. By contrast, suppression was not observed in mESCs expressing luc
Fir and GFP alone or when either GFP- or SID-1-GFP-expressing cells were incubated with control dsRNAs/siRNAs (non-silencing or
Renilla luciferase-specific). These results may lead to high-throughput experimental strategies for studying ESC differentiation and novel approaches to genetically inhibit or eliminate the tumorigenicity of ESCs. |
| doi_str_mv | 10.1016/j.bbrc.2007.03.187 |
| format | Article |
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Caenorhabditis elegans, involves sequence-specific mRNA degradation mediated by double-stranded RNAs (dsRNAs). Passive dsRNA uptake has been uniquely observed in
C. elegans due to the expression of systemic RNA interference defective-1 (SID-1). Here we investigated the ability of ectopic SID-1 expression to enable passive cellular uptake of short interfering RNA (siRNA) or double stranded RNA (dsRNA) in pluripotent mouse embryonic stem cells (mESCs). When SID-1-GFP and the Firefly luciferase reporter gene (luc
Fir) were co-expressed in mESCs, luc
Fir activity could be suppressed by simple incubation with dsRNAs/siRNAs that were designed to specifically target luc
Fir. By contrast, suppression was not observed in mESCs expressing luc
Fir and GFP alone or when either GFP- or SID-1-GFP-expressing cells were incubated with control dsRNAs/siRNAs (non-silencing or
Renilla luciferase-specific). These results may lead to high-throughput experimental strategies for studying ESC differentiation and novel approaches to genetically inhibit or eliminate the tumorigenicity of ESCs.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2007.03.187</identifier><identifier>PMID: 17434453</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Caenorhabditis elegans ; Caenorhabditis elegans Proteins - genetics ; Caenorhabditis elegans Proteins - metabolism ; Cell Line ; Ectopic expression ; Embryonic stem cells ; Embryonic Stem Cells - metabolism ; Gene Silencing - physiology ; Gene transfer ; Humans ; Kidney - embryology ; Kidney - metabolism ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Recombinant Proteins - metabolism ; Renilla ; RNA interference ; RNA Interference - physiology ; SID-1 ; Transfection - methods</subject><ispartof>Biochemical and biophysical research communications, 2007-06, Vol.357 (2), p.480-486</ispartof><rights>2007 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c550t-b1fe122cef528c28d61ad62399e2a0d8ccfb4f22da118a5004a71e3f0c4cfa163</citedby><cites>FETCH-LOGICAL-c550t-b1fe122cef528c28d61ad62399e2a0d8ccfb4f22da118a5004a71e3f0c4cfa163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2007.03.187$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17434453$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsang, Suk Ying</creatorcontrib><creatorcontrib>Moore, Jennifer C.</creatorcontrib><creatorcontrib>Huizen, Rika Van</creatorcontrib><creatorcontrib>Chan, Camie W.Y.</creatorcontrib><creatorcontrib>Li, Ronald A.</creatorcontrib><title>Ectopic expression of systemic RNA interference defective protein in embryonic stem cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>RNA interference (RNAi), a post-transcriptional gene silencing mechanism originally described in
Caenorhabditis elegans, involves sequence-specific mRNA degradation mediated by double-stranded RNAs (dsRNAs). Passive dsRNA uptake has been uniquely observed in
C. elegans due to the expression of systemic RNA interference defective-1 (SID-1). Here we investigated the ability of ectopic SID-1 expression to enable passive cellular uptake of short interfering RNA (siRNA) or double stranded RNA (dsRNA) in pluripotent mouse embryonic stem cells (mESCs). When SID-1-GFP and the Firefly luciferase reporter gene (luc
Fir) were co-expressed in mESCs, luc
Fir activity could be suppressed by simple incubation with dsRNAs/siRNAs that were designed to specifically target luc
Fir. By contrast, suppression was not observed in mESCs expressing luc
Fir and GFP alone or when either GFP- or SID-1-GFP-expressing cells were incubated with control dsRNAs/siRNAs (non-silencing or
Renilla luciferase-specific). These results may lead to high-throughput experimental strategies for studying ESC differentiation and novel approaches to genetically inhibit or eliminate the tumorigenicity of ESCs.</description><subject>Animals</subject><subject>Caenorhabditis elegans</subject><subject>Caenorhabditis elegans Proteins - genetics</subject><subject>Caenorhabditis elegans Proteins - metabolism</subject><subject>Cell Line</subject><subject>Ectopic expression</subject><subject>Embryonic stem cells</subject><subject>Embryonic Stem Cells - metabolism</subject><subject>Gene Silencing - physiology</subject><subject>Gene transfer</subject><subject>Humans</subject><subject>Kidney - embryology</subject><subject>Kidney - metabolism</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Recombinant Proteins - metabolism</subject><subject>Renilla</subject><subject>RNA interference</subject><subject>RNA Interference - physiology</subject><subject>SID-1</subject><subject>Transfection - methods</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkd9rFDEQx4Mo9mz9B3yQffJt15kk-wtEKKWtQlEQhfoUstmJ5rjdrMne0fvvm-UObV_qU2DmM18y82HsDUKBgNX7ddF1wRQcoC5AFNjUz9gKoYWcI8jnbAUAVc5bvD1hr2JcAyDKqn3JTrCWQspSrNjPSzP7yZmM7qZAMTo_Zt5mcR9nGlL525fzzI0zBUuBRkNZT5bM7HaUTcHP5MbUzmjowt6PiV_GMkObTTxjL6zeRHp9fE_Zj6vL7xef8puv158vzm9yU5Yw5x1aQs4N2ZI3hjd9hbqvuGhb4hr6xhjbSct5rxEbXQJIXSMJC0Yaq7ESp-zjIXfadgP1hsY56I2aght02CuvnXrcGd1v9cvvFJeV5K1IAe-OAcH_2VKc1eDisoIeyW-jqkFykOL_ILZ1nQ4LCeQH0AQfYyD79zcIalGn1mpRpxZ1CoRK6tLQ24d7_Bs5ukrAhwNA6Zo7R0FF4xYnvQtJieq9eyr_Huy7rSk</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Tsang, Suk Ying</creator><creator>Moore, Jennifer C.</creator><creator>Huizen, Rika Van</creator><creator>Chan, Camie W.Y.</creator><creator>Li, Ronald A.</creator><general>Elsevier Inc</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>7QO</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20070601</creationdate><title>Ectopic expression of systemic RNA interference defective protein in embryonic stem cells</title><author>Tsang, Suk Ying ; Moore, Jennifer C. ; Huizen, Rika Van ; Chan, Camie W.Y. ; Li, Ronald A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c550t-b1fe122cef528c28d61ad62399e2a0d8ccfb4f22da118a5004a71e3f0c4cfa163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Caenorhabditis elegans</topic><topic>Caenorhabditis elegans Proteins - genetics</topic><topic>Caenorhabditis elegans Proteins - metabolism</topic><topic>Cell Line</topic><topic>Ectopic expression</topic><topic>Embryonic stem cells</topic><topic>Embryonic Stem Cells - metabolism</topic><topic>Gene Silencing - physiology</topic><topic>Gene transfer</topic><topic>Humans</topic><topic>Kidney - embryology</topic><topic>Kidney - metabolism</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Recombinant Proteins - metabolism</topic><topic>Renilla</topic><topic>RNA interference</topic><topic>RNA Interference - physiology</topic><topic>SID-1</topic><topic>Transfection - methods</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsang, Suk Ying</creatorcontrib><creatorcontrib>Moore, Jennifer C.</creatorcontrib><creatorcontrib>Huizen, Rika Van</creatorcontrib><creatorcontrib>Chan, Camie W.Y.</creatorcontrib><creatorcontrib>Li, Ronald A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsang, Suk Ying</au><au>Moore, Jennifer C.</au><au>Huizen, Rika Van</au><au>Chan, Camie W.Y.</au><au>Li, Ronald A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ectopic expression of systemic RNA interference defective protein in embryonic stem cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>357</volume><issue>2</issue><spage>480</spage><epage>486</epage><pages>480-486</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>RNA interference (RNAi), a post-transcriptional gene silencing mechanism originally described in
Caenorhabditis elegans, involves sequence-specific mRNA degradation mediated by double-stranded RNAs (dsRNAs). Passive dsRNA uptake has been uniquely observed in
C. elegans due to the expression of systemic RNA interference defective-1 (SID-1). Here we investigated the ability of ectopic SID-1 expression to enable passive cellular uptake of short interfering RNA (siRNA) or double stranded RNA (dsRNA) in pluripotent mouse embryonic stem cells (mESCs). When SID-1-GFP and the Firefly luciferase reporter gene (luc
Fir) were co-expressed in mESCs, luc
Fir activity could be suppressed by simple incubation with dsRNAs/siRNAs that were designed to specifically target luc
Fir. By contrast, suppression was not observed in mESCs expressing luc
Fir and GFP alone or when either GFP- or SID-1-GFP-expressing cells were incubated with control dsRNAs/siRNAs (non-silencing or
Renilla luciferase-specific). These results may lead to high-throughput experimental strategies for studying ESC differentiation and novel approaches to genetically inhibit or eliminate the tumorigenicity of ESCs.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17434453</pmid><doi>10.1016/j.bbrc.2007.03.187</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 2007-06, Vol.357 (2), p.480-486 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Animals Caenorhabditis elegans Caenorhabditis elegans Proteins - genetics Caenorhabditis elegans Proteins - metabolism Cell Line Ectopic expression Embryonic stem cells Embryonic Stem Cells - metabolism Gene Silencing - physiology Gene transfer Humans Kidney - embryology Kidney - metabolism Membrane Proteins - genetics Membrane Proteins - metabolism Mice Recombinant Proteins - metabolism Renilla RNA interference RNA Interference - physiology SID-1 Transfection - methods |
| title | Ectopic expression of systemic RNA interference defective protein in embryonic stem cells |
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