The original antibody was raised by immunising mice with L-dsRNA
Conjugate
Unconjugated
Target
Alternative Names
double-stranded RNA; ds-RNA
Citations
Publication ()
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Background
Double-stranded RNA (dsRNA) is a double-helical structure composed of two complementary strands of RNA that is closely associated with most viral infections, either as the genetic material of dsRNA viruses or produced in large quantities during viral replication cycles. It plays a critical role in immune regulation, with nearly all organisms capable of recognizing and responding to dsRNA. Inside host cells, dsRNA replicates to generate new dsRNA genomes and mRNA. The resulting single-stranded mRNA is translated by host ribosomes into viral proteins, which assemble with new genomes to form viral particles released to infect the next cell.
dsRNA is pivotal in mediating RNA interference (RNAi), a key genetic mechanism. Upon entry into cells, long dsRNA is recognized and cleaved by an enzyme called Dicer into small interfering RNA (siRNA) or precursor microRNA (pre-miRNA) fragments, each about 20 nucleotides long. These fragments bind with proteins to form the RNA-induced silencing complex (RISC). Within RISC, the RNA duplex separates, with one strand guiding RISC to bind complementary target mRNA. This binding leads to mRNA degradation or prevents ribosome binding, thereby terminating protein translation and preventing the expression of specific genes. This gene silencing mechanism is crucial in gene function studies, antiviral research, and gene therapy development.
Currently, dsRNA's potential applications in agricultural production are widely studied. Leveraging the RNAi mechanism, introducing dsRNA into genetically modified (GM) crops can silence target genes, thereby enhancing crop characteristics and bolstering defenses against pests and diseases. Moreover, dsRNA has been shown to degrade rapidly with a half-life of less than 3 days and does not persist in aquatic systems, making it suitable for foliar spraying on plant surfaces. Due to its ability to enter insect cells efficiently via oral ingestion and its strict specificity, dsRNA presents a promising alternative to conventional insecticides as an effective, non-toxic, and sustainable approach to pest control. However, challenges remain in ensuring effective delivery, given limitations such as nuclease degradation and uptake efficiency.
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References
DsRNA-based pesticides: Considerations for efficiency and risk assessment
Chemosphere
Authors: Dalakouras, A. Koidou, V. Papadopoulou, K.
In view of the ongoing climate change and the ever-growing world population, novel agricultural solutions are required to ensure sustainable food supply. Microbials, natural substances, semiochemicals and double stranded RNAs (dsRNAs) are all considered potential low risk pesticides. DsRNAs function at the molecular level, targeting specific regions of specific genes of specific organisms, provided that they share a minimal sequence complementarity of approximately 20 nucleotides. Thus, dsRNAs may offer a great alternative to conventional chemicals in environmentally friendly pest control strategies. Any low-risk pesticide needs to be efficient and exhibit low toxicological potential and low environmental persistence. Having said that, in the current review, the mode of dsRNA action is explored and the parameters that need to be taken into consideration for the development of efficient dsRNA-based pesticides are highlighted. Moreover, since dsRNAs mode of action differs from those of synthetic pesticides, custom-made risk assessment schemes may be required and thus, critical issues related to the risk assessment of dsRNA pesticides are discussed here.
Novel insights into double-stranded RNA-mediated immunopathology
Recent progress in human and mouse genetics has transformed our understanding of the molecular mechanisms by which recognition of self double-stranded RNA (self-dsRNA) causes immunopathology. Novel mouse models recapitulate loss-of-function mutations in the RNA editing enzyme ADAR1 that are found in patients with Aicardi–Goutières syndrome (AGS) — a monogenic inflammatory disease associated with increased levels of type I interferon. Extensive analyses of the genotype–phenotype relationships in these mice have now firmly established a causal relationship between increased intracellular concentrations of endogenous immunostimulatory dsRNA and type I interferon-driven immunopathology. Activation of the dsRNA-specific immune sensor MDA5 perpetuates the overproduction of type I interferons, and chronic engagement of the interferon-inducible innate immune receptors PKR and ZBP1 by dsRNA drives immunopathology by activating an integrated stress response or by inducing excessive cell death. Biochemical and genetic data support a role for the p150 isoform of ADAR1 in the cytosol in suppressing the spontaneous, pathological response to self-dsRNA.