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Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
siRNA - Small Interfering RNAs02:30

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Ribozymes

The term ribozyme is used for RNA that can act as an enzyme. Ribozymes are mainly found in selected viruses, bacteria, plant organelles, and lower eukaryotes. Ribozymes were first discovered in 1982 when Tom Cech’s laboratory observed Group I introns acting as enzymes. This was shortly followed by the discovery of another ribozyme, Ribonulcease P, by Sid Altman’s laboratory. Both Cech and Altman received the Nobel Prize in chemistry in 1989 for their work on ribozymes.
Ribozymes can be...
RNA Interference01:23

RNA Interference

RNA interference (RNAi) is a process in which a small non-coding RNA molecule blocks the post-transcriptional expression of a gene by binding to its messenger RNA (mRNA) and preventing the protein from being translated.
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RNA Interference01:23

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Updated: Jun 20, 2026

Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells
07:23

Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells

Published on: May 30, 2025

Ribonucleases and immunoRNases as anticancer drugs.

S M Rybak1, M A E Arndt, T Schirrmann

  • 1Bionanomics, LLC, 411 Walnut Street, Green Cove Springs, FL 32043, USA. rybak@mindspring.com

Current Pharmaceutical Design
|August 20, 2009
PubMed
Summary
This summary is machine-generated.

Ribonucleases are emerging drug targets for cancer therapy. Researchers are developing immunoRNases, combining ribonucleases with antibodies, to specifically destroy tumor cells, offering a promising alternative to traditional immunotoxins.

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Sequence-specific and Selective Recognition of Double-stranded RNAs over Single-stranded RNAs by Chemically Modified Peptide Nucleic Acids

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Last Updated: Jun 20, 2026

Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells
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Kinetic Screening of Nuclease Activity using Nucleic Acid Probes
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Kinetic Screening of Nuclease Activity using Nucleic Acid Probes

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Sequence-specific and Selective Recognition of Double-stranded RNAs over Single-stranded RNAs by Chemically Modified Peptide Nucleic Acids
09:04

Sequence-specific and Selective Recognition of Double-stranded RNAs over Single-stranded RNAs by Chemically Modified Peptide Nucleic Acids

Published on: September 21, 2017

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Ribonucleases (RNases) are enzymes that degrade RNA.
  • RNases are increasingly recognized as important drug targets, particularly in cancer therapy.
  • The RNase superfamily includes enzymes like bovine pancreatic RNase A, angiogenin, and ONCONASE, each with distinct properties.

Purpose of the Study:

  • To explore the potential of RNases as therapeutic agents for cancer treatment.
  • To describe the development and properties of immunoRNases, a novel class of cancer therapeutics.
  • To compare the efficacy and construction of immunoRNases with traditional immunotoxins.

Main Methods:

  • Characterization of RNase superfamily members, including bovine pancreatic RNase A, angiogenin, and ONCONASE.
  • Generation of immunoRNases through chemical conjugation and recombinant fusion protein strategies.
  • Evaluation of RNase properties and their application as antibody payloads.

Main Results:

  • RNase-based therapeutics, specifically immunoRNases, have demonstrated efficacy in killing tumor cells both in vitro and in vivo.
  • ONCONASE has progressed to a Phase IIIb clinical trial for malignant mesothelioma.
  • ImmunoRNases offer a sophisticated approach to targeted cancer therapy.

Conclusions:

  • RNases represent a viable and potent class of therapeutic agents for cancer treatment.
  • ImmunoRNases provide a targeted delivery mechanism for cytotoxic RNases to cancer cells.
  • RNase-based strategies offer potential advantages over traditional immunotoxins in cancer therapy.