ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Discovery of SKP2-Recruiting PROTACs for Target Protein Degradation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Delivering Degradation: Nanomedicine and Programmable Proximity Platforms for Targeted Protein Degradation.Pharmaceutics · 2026Review
- SKP2 in Cancer: From Molecular Regulation to Therapeutic Vulnerabilities and Translational Perspectives.Drug design, development and therapy · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Proteolysis targeting chimeras (PROTACs) have emerged as an intriguing therapeutic strategy for targeted protein degradation (TPD), functioning as heterobifunctional compounds that induce the redirection of E3 ligases to ubiquitinate neo-substrates for proteasomal degradation. Despite the presence of over 600 E3 ligases, only a limited subset has been successfully harnessed for TPD. This study demonstrates that S-phase kinase-associated protein 2 (SKP2), the substrate receptor of the Cullin RING ligase 1 (CRL1) subfamily, can be employed for TPD using a selective, non-covalent SKP2 recruiter, SL1. We designed and synthesized SKP2-recruiting degraders by linking SL1 to the BRD4 inhibitor JQ1. These compounds effectively induce BRD4 degradation in MV-4-11 cells, with the most potent compound 2-1 exhibiting a half-maximal degradation (DC
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.