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Related Experiment Video

Updated: Mar 14, 2026

Biotin-based Pulldown Assay to Validate mRNA Targets of Cellular miRNAs

Biotin-based Pulldown Assay to Validate mRNA Targets of Cellular miRNAs

Published on: June 12, 2018

A druggable target for rescuing microRNA defects.

Ken Asada¹, Emanuele Canestrari¹, Zain Paroo²

¹Center for Pharmaceutical Biotechnology, University of Illinois at Chicago, Chicago, IL 60612, USA.

Bioorganic & Medicinal Chemistry Letters

|September 20, 2016

Summary

This summary is machine-generated.

Researchers identified inhibitors for the Translin/Trax (TN/TX) enzyme complex, which degrades microRNA precursors. This discovery offers a new therapeutic strategy for microRNA (miRNA) defects by enhancing miRNA processing.

Keywords:

Dicer High-throughput screen Small molecule Translin Trax miRNA therapeutics

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Last Updated: Mar 14, 2026

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Identifying Targets of Human microRNAs with the LightSwitch Luciferase Assay System using 3'UTR-reporter Constructs and a microRNA Mimic in Adherent Cells

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Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library

Published on: April 6, 2012

Area of Science:

Biochemistry
Molecular Biology
Pharmacology

Background:

MicroRNA (miRNA) therapeutics face pharmacodynamic challenges, limiting oligonucleotide-based approaches.
Enzymes regulating miRNA metabolism are emerging as potential therapeutic targets.
The Translin/Trax (TN/TX) ribonuclease complex degrades pre-miRNA, competing with Dicer processing.

Purpose of the Study:

To establish a high-throughput assay for identifying TN/TX inhibitors.
To screen a library of compounds for TN/TX inhibitory activity.
To evaluate the therapeutic potential of inhibiting TN/TX for miRNA pathway modulation.

Main Methods:

Developed and implemented a high-throughput screening assay for the TN/TX ribonuclease complex.
Screened 2320 drug and natural product compounds against TN/TX.
Conducted secondary analyses to confirm TN/TX inhibition and its effect on miRNA processing.

Main Results:

Identified small molecule inhibitors of the TN/TX enzyme complex.
Demonstrated that these inhibitors reduce pre-miRNA degradation by TN/TX.
Showed enhanced miRNA processing by Dicer in the presence of TN/TX inhibitors.

Conclusions:

Established TN/TX as a druggable target for rescuing global miRNA defects.
This approach complements existing miRNA therapeutic strategies.
Demonstrated the feasibility of pharmacologically targeting the 'ribonucleome' for therapeutic benefit.