Synthetic dsRNA Dicer substrates enhance RNAi potency and efficacy.
Identifieur interne : 002352 ( PubMed/Curation ); précédent : 002351; suivant : 002353Synthetic dsRNA Dicer substrates enhance RNAi potency and efficacy.
Auteurs : Dong-Ho Kim ; Mark A. Behlke ; Scott D. Rose ; Mi-Sook Chang ; Sangdun Choi ; John J. RossiSource :
- Nature biotechnology [ 1087-0156 ] ; 2005.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Petit ARN interférent, Régulation de l'expression des gènes.
- métabolisme : Ribonuclease III.
- physiologie : Extinction de l'expression des gènes.
- Ciblage de gène, Génie génétique, Petit ARN interférent, Ribonuclease III, Transfection.
English descriptors
- KwdEn :
- MESH :
- chemical , chemistry : RNA, Small Interfering, Ribonuclease III.
- genetics : Gene Expression Regulation, RNA, Small Interfering.
- chemical , metabolism : Ribonuclease III.
- methods : Gene Targeting, Genetic Engineering, Transfection.
- physiology : Gene Silencing.
Abstract
RNA interference (RNAi) is the process of sequence-specific post-transcriptional gene silencing triggered by double-stranded RNAs. In attempts to identify RNAi triggers that effectively function at lower concentrations, we found that synthetic RNA duplexes 25-30 nucleotides in length can be up to 100-fold more potent than corresponding conventional 21-mer small interfering RNAs (siRNAs). Some sites that are refractory to silencing by 21-mer siRNAs can be effectively targeted by 27-mer duplexes, with silencing lasting up to 10 d. Notably, the 27-mers do not induce interferon or activate protein kinase R (PKR). The enhanced potency of the longer duplexes is attributed to the fact that they are substrates of the Dicer endonuclease, directly linking the production of siRNAs to incorporation in the RNA-induced silencing complex. These results provide an alternative strategy for eliciting RNAi-mediated target cleavage using low concentrations of synthetic RNA as substrates for cellular Dicer-mediated cleavage.
DOI: 10.1038/nbt1051
PubMed: 15619617
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: Pour aller vers cette notice dans l'étape Curation :002352
Links to Exploration step
pubmed:15619617Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Synthetic dsRNA Dicer substrates enhance RNAi potency and efficacy.</title><author><name sortKey="Kim, Dong Ho" sort="Kim, Dong Ho" uniqKey="Kim D" first="Dong-Ho" last="Kim">Dong-Ho Kim</name></author><author><name sortKey="Behlke, Mark A" sort="Behlke, Mark A" uniqKey="Behlke M" first="Mark A" last="Behlke">Mark A. Behlke</name></author><author><name sortKey="Rose, Scott D" sort="Rose, Scott D" uniqKey="Rose S" first="Scott D" last="Rose">Scott D. Rose</name></author><author><name sortKey="Chang, Mi Sook" sort="Chang, Mi Sook" uniqKey="Chang M" first="Mi-Sook" last="Chang">Mi-Sook Chang</name></author><author><name sortKey="Choi, Sangdun" sort="Choi, Sangdun" uniqKey="Choi S" first="Sangdun" last="Choi">Sangdun Choi</name></author><author><name sortKey="Rossi, John J" sort="Rossi, John J" uniqKey="Rossi J" first="John J" last="Rossi">John J. Rossi</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15619617</idno><idno type="pmid">15619617</idno><idno type="doi">10.1038/nbt1051</idno><idno type="wicri:Area/PubMed/Corpus">002352</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002352</idno><idno type="wicri:Area/PubMed/Curation">002352</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">002352</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Synthetic dsRNA Dicer substrates enhance RNAi potency and efficacy.</title><author><name sortKey="Kim, Dong Ho" sort="Kim, Dong Ho" uniqKey="Kim D" first="Dong-Ho" last="Kim">Dong-Ho Kim</name></author><author><name sortKey="Behlke, Mark A" sort="Behlke, Mark A" uniqKey="Behlke M" first="Mark A" last="Behlke">Mark A. Behlke</name></author><author><name sortKey="Rose, Scott D" sort="Rose, Scott D" uniqKey="Rose S" first="Scott D" last="Rose">Scott D. Rose</name></author><author><name sortKey="Chang, Mi Sook" sort="Chang, Mi Sook" uniqKey="Chang M" first="Mi-Sook" last="Chang">Mi-Sook Chang</name></author><author><name sortKey="Choi, Sangdun" sort="Choi, Sangdun" uniqKey="Choi S" first="Sangdun" last="Choi">Sangdun Choi</name></author><author><name sortKey="Rossi, John J" sort="Rossi, John J" uniqKey="Rossi J" first="John J" last="Rossi">John J. Rossi</name></author></analytic><series><title level="j">Nature biotechnology</title><idno type="ISSN">1087-0156</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Gene Expression Regulation (genetics)</term><term>Gene Silencing (physiology)</term><term>Gene Targeting (methods)</term><term>Genetic Engineering (methods)</term><term>RNA, Small Interfering (chemistry)</term><term>RNA, Small Interfering (genetics)</term><term>Ribonuclease III (chemistry)</term><term>Ribonuclease III (metabolism)</term><term>Transfection (methods)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Ciblage de gène ()</term><term>Extinction de l'expression des gènes (physiologie)</term><term>Génie génétique ()</term><term>Petit ARN interférent ()</term><term>Petit ARN interférent (génétique)</term><term>Ribonuclease III ()</term><term>Ribonuclease III (métabolisme)</term><term>Régulation de l'expression des gènes (génétique)</term><term>Transfection ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>RNA, Small Interfering</term><term>Ribonuclease III</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Expression Regulation</term><term>RNA, Small Interfering</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Petit ARN interférent</term><term>Régulation de l'expression des gènes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Ribonuclease III</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Gene Targeting</term><term>Genetic Engineering</term><term>Transfection</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Ribonuclease III</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Extinction de l'expression des gènes</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Silencing</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Ciblage de gène</term><term>Génie génétique</term><term>Petit ARN interférent</term><term>Ribonuclease III</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">RNA interference (RNAi) is the process of sequence-specific post-transcriptional gene silencing triggered by double-stranded RNAs. In attempts to identify RNAi triggers that effectively function at lower concentrations, we found that synthetic RNA duplexes 25-30 nucleotides in length can be up to 100-fold more potent than corresponding conventional 21-mer small interfering RNAs (siRNAs). Some sites that are refractory to silencing by 21-mer siRNAs can be effectively targeted by 27-mer duplexes, with silencing lasting up to 10 d. Notably, the 27-mers do not induce interferon or activate protein kinase R (PKR). The enhanced potency of the longer duplexes is attributed to the fact that they are substrates of the Dicer endonuclease, directly linking the production of siRNAs to incorporation in the RNA-induced silencing complex. These results provide an alternative strategy for eliciting RNAi-mediated target cleavage using low concentrations of synthetic RNA as substrates for cellular Dicer-mediated cleavage.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15619617</PMID><DateCompleted><Year>2005</Year><Month>05</Month><Day>31</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1087-0156</ISSN><JournalIssue CitedMedium="Print"><Volume>23</Volume><Issue>2</Issue><PubDate><Year>2005</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Nature biotechnology</Title><ISOAbbreviation>Nat. Biotechnol.</ISOAbbreviation></Journal><ArticleTitle>Synthetic dsRNA Dicer substrates enhance RNAi potency and efficacy.</ArticleTitle><Pagination><MedlinePgn>222-6</MedlinePgn></Pagination><Abstract><AbstractText>RNA interference (RNAi) is the process of sequence-specific post-transcriptional gene silencing triggered by double-stranded RNAs. In attempts to identify RNAi triggers that effectively function at lower concentrations, we found that synthetic RNA duplexes 25-30 nucleotides in length can be up to 100-fold more potent than corresponding conventional 21-mer small interfering RNAs (siRNAs). Some sites that are refractory to silencing by 21-mer siRNAs can be effectively targeted by 27-mer duplexes, with silencing lasting up to 10 d. Notably, the 27-mers do not induce interferon or activate protein kinase R (PKR). The enhanced potency of the longer duplexes is attributed to the fact that they are substrates of the Dicer endonuclease, directly linking the production of siRNAs to incorporation in the RNA-induced silencing complex. These results provide an alternative strategy for eliciting RNAi-mediated target cleavage using low concentrations of synthetic RNA as substrates for cellular Dicer-mediated cleavage.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Dong-Ho</ForeName><Initials>DH</Initials></Author><Author ValidYN="Y"><LastName>Behlke</LastName><ForeName>Mark A</ForeName><Initials>MA</Initials></Author><Author ValidYN="Y"><LastName>Rose</LastName><ForeName>Scott D</ForeName><Initials>SD</Initials></Author><Author ValidYN="Y"><LastName>Chang</LastName><ForeName>Mi-Sook</ForeName><Initials>MS</Initials></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Sangdun</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Rossi</LastName><ForeName>John J</ForeName><Initials>JJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI29329</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI42552</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL074704</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016422">Letter</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2004</Year><Month>12</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Nat Biotechnol</MedlineTA><NlmUniqueID>9604648</NlmUniqueID><ISSNLinking>1087-0156</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.26.3</RegistryNumber><NameOfSubstance UI="D043244">Ribonuclease III</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Nat Biotechnol. 2005 Feb;23(2):181-2</RefSource><PMID Version="1">15696144</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020868" MajorTopicYN="N">Gene Silencing</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018390" MajorTopicYN="N">Gene Targeting</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005818" MajorTopicYN="N">Genetic Engineering</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D043244" MajorTopicYN="N">Ribonuclease III</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2004</Year><Month>07</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2004</Year><Month>11</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>12</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>6</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>12</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15619617</ArticleId><ArticleId IdType="pii">nbt1051</ArticleId><ArticleId IdType="doi">10.1038/nbt1051</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/MersV1/Data/PubMed/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002352 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd -nk 002352 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= MersV1
|flux= PubMed
|étape= Curation
|type= RBID
|clé= pubmed:15619617
|texte= Synthetic dsRNA Dicer substrates enhance RNAi potency and efficacy.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:15619617" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a MersV1
| This area was generated with Dilib version V0.6.33. |  |