Stefan Kubicek

This study identifies three small molecule inhibitors that reduce macrophage survival and viability, showing therapeutic potential in models of inflammation and cancer.

This study establishes a murine tumoroid biobank to identify oncogenic pathways and drug vulnerabilities in prostate cancer, finding that PTEN loss drives cancer pathways and that specific compounds inhibit tumor growth.

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 CD8+ T cells drive energy substrate redistribution between lymphoid organs and the heart during viral infection, with metabolic adaptations affecting cardiac function.

This study identifies purine nucleobases as immunometabolites that enhance CD8+ T cell effector function by enabling a metabolic switch from de novo synthesis to salvage pathway.

The paper quantifies proteins directly interacting with DNA in human cells and identifies key transcription factors and DNA damage proteins in response to treatments.

The paper identifies a non-enzymatic role of NUDT5 in repressing purine de novo synthesis by scaffolding PPAT, with implications for cancer treatment and MTHFD1 deficiency.

The paper develops NUDT5 degraders and shows NUDT5 has a non-enzymatic role in 6-TG toxicity, distinct from NUDT15.

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 kinase-specific vulnerabilities and resistances in response to DNA damaging agents using kinase-deficient cell lines and validates gene-drug interactions.

The paper identifies insulin-independent modulators of glucose metabolism using a zebrafish model and finds androgen receptor antagonists reduce fasting glucose levels in insulin mutants.