Georg E. Winter

A parallelized BindCraft pipeline generated 306,146 in silico binder candidates against 8,296 human proteins, each with sequence, predicted complex and confidence metrics, freely accessible online.

This study shows that SERDs induce ER SUMOylation, which recruits co-repressors to suppress transcription, rather than relying on ER degradation for their activity.

The paper identifies epimerized host-derived bile acids as a driver of dysbiosis in IBD by selecting for bile-resistant bacteria that disrupt host bile acid feedback signaling.

The paper identifies SAGA CORE subunits as essential for KAT2A stability, showing that their disruption leads to proteasomal degradation of KAT2A and reduced H3K9 acetylation.

This paper introduces TRIPs, neomorphic molecules that recruit BAF complexes to rewire BCL6 in DLBCL, inducing apoptosis through chromatin remodeling.

The paper identifies V-ATPase inhibition as a trigger for apoptosis via GCN1/GCN2 kinase signaling and MCL-1 depletion, revealing a therapeutic target in certain cancers.

This study uses high-throughput chemistry to discover chemical inducers of proximity by modifying pre-existing ligands and screening for degrader activity.

The paper identifies iDegs, which enhance IDO1 degradation via the native CRL2KLHDC3 pathway, reducing kynurenine formation and offering new therapeutic potential for cancer.

The paper identifies inhibitor-induced kinase destabilization as a common phenomenon and reveals that it occurs through endogenous proteolytic mechanisms rather than classical ubiquitination.

This study shows that a monovalent MGD can recruit two E3 ligases redundantly to degrade SMARCA2/4, with tunable ligase preference through chemical and genetic modifications.

The paper introduces a method to identify direct protein substrates of small-molecule degraders using degradome analysis and mass spectrometry.

This paper develops a scalable method to identify E3-specific degraders by tracing substrate receptor abundance changes induced by pharmacological auto-degradation.

The paper identifies functional E3 ligase hotspots and resistance mechanisms to small-molecule degraders using haploid genetics and deep mutational scanning.