Journal
NATURE BIOTECHNOLOGY
Volume 27, Issue 3, Pages 257-263Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nbt.1525
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Funding
- National Institutes of Health [GM057286, CA119934, R43GM085863]
- Gunderson lab
- Rutgers University/University of Medicine and Dentistry New Jersey RNA community
- IDT corporation
- NATIONAL CANCER INSTITUTE [R21CA119934] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R43GM085863, R01GM057286] Funding Source: NIH RePORTER
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We describe a gene silencing method that employs a mechanism of action distinct from those of antisense and RNA interference. U1 Adaptors are bifunctional oligonucleotides with a 'target domain' complementary to a site in the target gene's terminal exon and a 'U1 domain' that binds to the U1 small nuclear RNA component of the U1 small nuclear ribonucleoprotein (U1 snRNP) splicing factor. Tethering of U1 snRNP to the target pre-mRNA inhibits poly(A)-tail addition, causing degradation of that RNA species in the nucleus. U1 Adaptors can inhibit both endogenous and reporter genes in a sequence-specific manner. Comparison of U1 Adaptors with small interfering RNA (siRNA) using a genome-wide microarray analysis indicates that U1 Adaptors have limited off-target effects and no detectable adverse effects on splicing. Further, targeting the same gene either with multiple U1 Adaptors or with a U1 Adaptor and siRNA strongly enhances gene silencing.
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