A trial of mitofusin activation shows neuron regeneration and phenotype reversal in vitro and in vivo in experimental Charcot–Marie–Tooth disease type 2A caused by mitofusin 2 mutations.

The developmental transcription factor TBX3 co-operates with β-catenin co-factors to operate tissue-specific transcriptional outputs, during forelimb development and colorectal cancer progression.

MARCH5 mediates a pathway driving MCL1 degradation in response to cellular stress, which sensitizes to BH3 mimetic drugs targeting BCLXL and provides a broadly effective therapeutic strategy for solid tumors.

Targeting the CRL5 ubiquitin ligase complex in combination with CDK9 or MCL1 inhibition could combat innate and acquired resistance of cancer cells to MCL1-targeting therapeutics.

The pro-apoptotic BH3-protein Bim contains two distinct binding sites for anti-apoptotic proteins that together confer resistance of Bim/Bcl-2 and Bim/Bcl-XL complexes to BH3-mimetic drugs under development for use in humans.

Disruptions to eye field size have little impact on final eye size due to tissue compensatory mechanisms.

Dimers of Bak assemble into clusters without using a distinct protein-protein interface, which may explain the apparent difficulties in obtaining high resolution structures of the pore complex and in targeting dimer-dimer interactions to regulate apoptosis.

Genetic and biochemical analysis reveals that MAPK signaling promotes axon degeneration by modulating the turnover of axon-protective proteins.

Six computationally designed and in vitro optimized protein inhibitors serve as molecular probes to reveal BCL2 profiles of different human cancers.

Libraries of patient-derived tumor organoids are a reliable and scalable model system that can help identify and optimize targeted therapies in a pre-clinical setting.