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  Analysis of gene function in somatic mammalian cells using small interfering RNAs

Elbashir, S. M., Harborth, J., Weber, K., & Tuschl, T. (2002). Analysis of gene function in somatic mammalian cells using small interfering RNAs. Methods, 26(2), 199-213. Retrieved from http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6WN5-45WGJF8-F-1P&_cdi=6953&_user=38661&_pii=S1046202302000233&_origin=search&_coverDate=02%2F28%2F2002&_sk=999739997&view=c&wchp=dGLbVtz-zSkWA&md5=c94da4baa1bbe2a59c130b0ea900a490&ie=/sdarticle.pdf.

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 Creators:
Elbashir, S. M.1, Author           
Harborth, J.2, Author           
Weber, K.2, Author           
Tuschl, T.1, Author           
Affiliations:
1Research Group of Combinatorical Biochemistry, MPI for biophysical chemistry, Max Planck Society, ou_578556              
2Department of Biochemistry and Cell Biology, MPI for biophysical chemistry, Max Planck Society, ou_578618              

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Free keywords: RNA interference; small interfering RNA; posttranscriptional gene silencing; knockdown; double-stranded RNA
 Abstract: RNA interference (RNAi) is a highly conserved gene silencing mechanism that uses double-stranded RNA (dsRNA) as a signal to trigger the degradation of homologous mRNA. The mediators of sequence-specific mRNA degradation are 21- to 23-nt small interfering RNAs (siRNAs) generated by ribonuclease III cleavage from longer dsRNAs. Twenty-one-nuclcotide siRNA duplexes trigger specific gene silencing in mammalian somatic cells without activation of the unspecific interferon response. Here we provide a collection of protocols for siRNA-mediated knockdown of mammalian gene expression. Because of the robustness of the siRNA knockdown technology. genomewide analysis of human gene function in cultured cells has now become possible. (C) 2002 Elsevier Science (USA). All rights reserved.

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Language(s): eng - English
 Dates: 2002-02
 Publication Status: Issued
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 Rev. Type: Peer
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Title: Methods
Source Genre: Journal
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Pages: - Volume / Issue: 26 (2) Sequence Number: - Start / End Page: 199 - 213 Identifier: -