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Effective Gene Silencing Tools

siRNAs are effective gene-silencing tools delivered via lentivirus, AAV, plasmids, or dsRNA transfection. Our dual-promoter system eliminates the need for hairpin shRNA design, simplifying cloning and target gene knockdown.

Lentivirus siRNA Library

abm’s lentiviral RNAi Expression System enables efficient siRNA delivery via transfection or infection. Its convergent promoter design improves gene knockdown without requiring hairpin structures. A broad library of human, mouse, and rat siRNAs is available in vector or pre-packaged lentivirus formats. 

Advantages
  • Potent 27–29 bp siRNAs vs traditional 19–21 bp 
  • Convergent promoters simplify cloning and sequencing
  • Optional GFP reporter for real-time monitoring
  • Available as 4-construct sets for stronger knockdown 
siRNA Vector Map

AAV siRNA Library

abm’s RNAi Expression System is available in AAV format, enabling efficient siRNA expression with non-integrating delivery for gene therapy.

Advantages of AAV siRNA
  • 27–29 bp siRNAs for stronger knockdown
  • Convergent promoters remove need for hairpin structures
  • GFP reporter for real-time monitoring
  • 3-construct pooled sets for improved silencing
  • Low immunogenicity with no genomic integration

pAAV siRNA GFP

siRNA dsRNA Oligo Library

siRNAs enable rapid, transient gene knockdown via dsRNA delivery without altering the genome. Suitable for in vitro and in vivo use, ABM offers pre-designed 3-siRNA sets for any human, mouse, or rat gene, plus controls.

Key Features:
  • Produced under ISO9000 standards.
  • Chemically modified (2’-OMe) for increased stability and lower toxicity.
  • 19-23 bases for each duplex in lyophilized format.
  • Set of 3 siRNA oligo duplexes for enhanced gene knockdown.
  • Included positive and negative controls.
  • Guaranteed knockdown of at least 70% in every set.

Resources

Resources iLenti siRNA Expressions ManualLenti-siRNA Expression Systems Manual Click Here to Download

Publications

Publication 1

Hepatic TET3 contributes to type-2 diabetes by inducing the HNF4α fetal isoform, Da Li et al., Nature Communications (2020) Click Here

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Contact our team today to request a quote or to reach out for personalised recommendations based on your research goals.