Michael Rapé

The paper shows proteasomes degrade repressive transcription factors, freeing chromatin for activator binding and enabling gene expression and cell fate decisions.

The paper shows cells use a ternary molecular glue to sense heme, triggering BACH1 degradation and HMOX1 expression to detoxify cytoplasmic heme while sparing mitochondrial heme, revealing a therapeutic vulnerability in AML.

This study identifies purine nucleotides as molecular glues that regulate purine biosynthesis by tethering PPAT to NUDT5, and shows how thiopurine drugs function as metabolic glues with enhanced potency.

This study identifies PP2A-A as a target of CRL3KBTBD4, showing that KBTBD4 mutations disrupt PP2A quality control and contribute to medulloblastoma by altering phospho-dependent signaling.

This study identifies TRIP12 as a key regulator of NRF2 degradation during oxidative stress recovery, showing it accelerates stress response silencing but limits NRF2 activation.

The paper reveals a temporal control mechanism driven by coupled ribosomes that enables the formation of intertwined protein dimers by bypassing closed monomeric states.

This study identifies CUL3-BTBD9 as an E3 ubiquitin ligase essential for myogenesis by ubiquitylating CAV1 and regulating insulin signaling in myoblasts.

This study determines the structure of the human E3 ligase SIFI, revealing its mechanism for ubiquitinating multiple substrates to silence the integrated stress response.

The paper identifies a poxvirus effector that triggers an NF-κB response by disrupting anti-viral complexes, revealing a novel ETI pathway.