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dc.contributor.authorPersengiev, Stephan P.
dc.contributor.authorZhu, Xiaochun
dc.contributor.authorGreen, Michael R.
dc.date2022-08-11T08:09:35.000
dc.date.accessioned2022-08-23T16:36:23Z
dc.date.available2022-08-23T16:36:23Z
dc.date.issued2003-12-19
dc.date.submitted2009-03-31
dc.identifier.citation<p>RNA. 2004 Jan;10(1):12-8.</p>
dc.identifier.issn1355-8382 (Print)
dc.identifier.pmid14681580
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38776
dc.description.abstractRNA interference is an evolutionarily conserved process in which expression of a specific gene is post-transcriptionally inhibited by a small interfering RNA (siRNA), which recognizes a complementary mRNA and induces its degradation. Currently, RNA interference is being used extensively to inhibit expression of specific genes for experimental and therapeutic purposes. For applications in mammalian cells, siRNAs are designed to be (dsRNA)-dependent protein kinase (PKR) response. Here we perform expression profiling in mammalian tissue-culture cells treated under standard conditions with conventional 21-bp siRNAs and find, unexpectedly, that >1000 genes involved in diverse cellular functions are nonspecifically stimulated or repressed. The effects on gene expression are dependent upon siRNA concentration and are stable throughout the course of siRNA treatment. Our results can be explained by previous studies showing that dsRNAs can affect multiple signaling and transcription pathways in addition to PKR. The potential for this widespread, nonspecific effect on mammalian gene expression must be carefully considered in the design of siRNA experiments and therapeutic applications.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=14681580&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1370513/
dc.subjectGene Expression Profiling
dc.subjectGene Expression Regulation
dc.subject*Gene Silencing
dc.subjectHela Cells
dc.subjectHumans
dc.subjectLuciferases
dc.subjectOligonucleotide Array Sequence Analysis
dc.subject*RNA Interference
dc.subjectRNA, Double-Stranded
dc.subjectRNA, Neoplasm
dc.subjectRNA, Small Interfering
dc.subjectReverse Transcriptase Polymerase Chain Reaction
dc.subjectTranscription, Genetic
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleNonspecific, concentration-dependent stimulation and repression of mammalian gene expression by small interfering RNAs (siRNAs)
dc.typeJournal Article
dc.source.journaltitleRNA (New York, N.Y.)
dc.source.volume10
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1622
dc.identifier.contextkey805443
html.description.abstract<p>RNA interference is an evolutionarily conserved process in which expression of a specific gene is post-transcriptionally inhibited by a small interfering RNA (siRNA), which recognizes a complementary mRNA and induces its degradation. Currently, RNA interference is being used extensively to inhibit expression of specific genes for experimental and therapeutic purposes. For applications in mammalian cells, siRNAs are designed to be (dsRNA)-dependent protein kinase (PKR) response. Here we perform expression profiling in mammalian tissue-culture cells treated under standard conditions with conventional 21-bp siRNAs and find, unexpectedly, that >1000 genes involved in diverse cellular functions are nonspecifically stimulated or repressed. The effects on gene expression are dependent upon siRNA concentration and are stable throughout the course of siRNA treatment. Our results can be explained by previous studies showing that dsRNAs can affect multiple signaling and transcription pathways in addition to PKR. The potential for this widespread, nonspecific effect on mammalian gene expression must be carefully considered in the design of siRNA experiments and therapeutic applications.</p>
dc.identifier.submissionpathoapubs/1622
dc.contributor.departmentProgram in Gene Function and Expression
dc.contributor.departmentHoward Hughes Medical Institute, Program in Molecular Medicine
dc.source.pages12-8


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