A second anti-apoptotic protein binding site in PUMA confers resistance to BH3 mimetic drugs and binds the protein to membranes.

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.

A subset of genes in the mouse brain show dynamically regulated and unequal expression of maternally and paternally derived variants, with implications for brain development and function.

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.

Short peptides that bind tightly to anti-apoptotic protein Bfl-1 but not other Bcl-2 family members provide a tool for diagnosing cancer cell survival mechanisms and a lead for developing new therapeutics.

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.

The C-terminal membrane binding domain of Bim is shown to interact with and activate Bim enabling it to kill cells not dependent on anti-apoptotic proteins for survival.

During ES cell differentiation, Yap1 directly regulates apoptosis-related genes like Bcl-2 and Mcl-1 to attenuate apoptosis and promote cell survival to allow for successful cell fate changes.

PPM1D-mutant leukemia cells exhibit a dysregulated redox landscape, a diminished response to oxidative stress, and rely on SOD1 for their survival.