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Related Experiment Video

Updated: Nov 4, 2025

Exploring Sequence Space to Identify Binding Sites for Regulatory RNA-Binding Proteins

Exploring Sequence Space to Identify Binding Sites for Regulatory RNA-Binding Proteins

Published on: August 9, 2019

A PROTAC targets splicing factor 3B1.

Rodrigo A Gama-Brambila¹, Jie Chen¹, Jun Zhou²

¹Buchmann Institute for Molecular Life Sciences, Pharmaceutical Chemistry, Goethe University Frankfurt am Main, Max-von-Laue-Strasse 15. R. 3.652, 60438 Frankfurt am Main, Germany.

Cell Chemical Biology

|May 28, 2021

Summary

This summary is machine-generated.

This study shows splicing factor 3B subunit 1 (SF3B1) can be degraded using proteolysis-targeting chimeras (PROTACs). This new PROTAC technology expands the range of targetable proteins for therapeutic development.

Keywords:

CRBN PROTAC SF3B1 inhibitor chemically induced protein-protein interaction molecular degrader proteomics proximity-based drug splicing factor 3B1 targeted protein degradation thalidomide

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Published on: June 30, 2022

Area of Science:

Biochemistry
Molecular Biology
Drug Discovery

Background:

Proteolysis-targeting chimeras (PROTACs) offer a novel therapeutic strategy for protein degradation.
Clinical applications of PROTACs are currently limited by the availability of chemical binders for specific target proteins.
The targetability of splicing factor 3B subunit 1 (SF3B1) by PROTACs remains unexplored.

Purpose of the Study:

To investigate if SF3B1 can be targeted by PROTACs.
To develop a novel PROTAC targeting SF3B1.
To evaluate the efficacy of the SF3B1-targeting PROTAC in cellular and in vivo models.

Main Methods:

Proteomic analysis of a novel compound O4I2 to identify its protein targets.
Chemical synthesis of a PROTAC (PROTAC-O4I2) by fusing O4I2 with thalidomide, a cereblon (CRBN) ligand.
Assessment of SF3B1 degradation, apoptosis induction, and efficacy in a Drosophila intestinal tumor model.

Main Results:

Proteomic analysis identified SF3B1 as a target of O4I2, which positively regulates RNA splicing.
PROTAC-O4I2 selectively degraded SF3B1 in a CRBN-dependent manner, inducing cellular apoptosis.
PROTAC-O4I2 treatment improved survival in a Drosophila intestinal tumor model by inhibiting stem cell maintenance and proliferation.

Conclusions:

SF3B1 is a targetable protein for PROTAC-mediated degradation.
Non-inhibitory chemical binders can be utilized to develop PROTACs.
This study expands the repertoire of targetable proteins for PROTAC technology, opening new avenues for therapeutic development.