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.
Authors
- Darci J. Trader (ORCID: https://orcid.org/0000-0002-0607-1243)
- Cody A. Loy (ORCID: https://orcid.org/0009-0004-9485-3174)
- Timothy J. Harris (ORCID: https://orcid.org/0009-0007-6273-2994)
- Laurence J. Seabrook (ORCID: https://orcid.org/0000-0002-9337-9712)
- Lauren V. Albrecht (ORCID: https://orcid.org/0000-0002-3147-8010)
- Eslam M.H. Ali (ORCID: https://orcid.org/0000-0003-3130-7630)
- Kate A. Kragness
Institutions
- University of California System (US)
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
- University of California, Irvine
- Chao Family Comprehensive Cancer Center