ByeTAC: Bypassing E-Ligase-Targeting Chimeras for Direct Proteasome Degradation

The development of targeted protein degradation by recruiting a protein of interest to a ubiquitin ligase to facilitate its degradation has become a powerful therapeutic tool. The potential of this approach is limited to proteins that can be readily ubiquitinated and relies on having a ligand with the various E3 ligases. Here, we describe a new methodology for targeted protein degradation that directly recruits a protein of interest to the proteasome for degradation. We generated bifunctional molecules that incorporate a small molecule ligand into a subunit on the 26S proteasome that recruits the protein directly for degradation. ByeTAC degradation requires binding to Rpn-13, a nonessential ubiquitin receptor of the 26S proteasome, and the protein of interest and does not have to rely on the E ligase cascade for ubiquitination. The ByeTAC methodology demonstrates the application of directly recruiting a protein to the proteasome via interactions with Rpn-13 for degradation.

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Publication Details

Journal
Journal of Medicinal Chemistry
Published
2025-04-19
DOI
https://doi.org/10.1021/acs.jmedchem.5c00485
Citations
18
Primary Topic
Protein Degradation and Inhibitors
Type
article
Field-Weighted Citation Impact
14.51

Funders

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article

ByeTAC: Bypassing E-Ligase-Targeting Chimeras for Direct Proteasome Degradation

Darci J. Trader, Cody A. Loy, Timothy J. Harris, Laurence J. Seabrook et al.
18 citations
Journal of Medicinal Chemistry
Protein Degradation and Inhibitors
14.51
article

ByeTAC: Bypassing E-Ligase-Targeting Chimeras for Direct Proteasome Degradation

Darci J. Trader, Cody A. Loy, Timothy J. Harris, Laurence J. Seabrook, Lauren V. Albrecht, Eslam M.H. Ali, Kate A. Kragness
article en
18 citations

Abstract

The development of targeted protein degradation by recruiting a protein of interest to a ubiquitin ligase to facilitate its degradation has become a powerful therapeutic tool. The potential of this approach is limited to proteins that can be readily ubiquitinated and relies on having a ligand with the various E3 ligases. Here, we describe a new methodology for targeted protein degradation that directly recruits a protein of interest to the proteasome for degradation. We generated bifunctional molecules that incorporate a small molecule ligand into a subunit on the 26S proteasome that recruits the protein directly for degradation. ByeTAC degradation requires binding to Rpn-13, a nonessential ubiquitin receptor of the 26S proteasome, and the protein of interest and does not have to rely on the E ligase cascade for ubiquitination. The ByeTAC methodology demonstrates the application of directly recruiting a protein to the proteasome via interactions with Rpn-13 for degradation.

Journal of Medicinal ChemistryVol. 68(9)
University of California System (US)
University of California, Irvine, Chao Family Comprehensive Cancer Center
Zero hunger
Openalex Percentile: Top 1%
Protein Degradation and Inhibitors
14.51
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ByeTAC: Bypassing E-Ligase-Targeting Chimeras for Direct Proteasome Degradation — Darci J. Trader, Cody A. Loy, et al. · Journal of Medicinal Chemistry (2025) | TGRS Research Map | TGRS