As the formation of BAX and BAK homo-oligomers strongly correlates with their ability to perforate mitochondria, defining how BAX and BAK dimers self-associate and interact with the membrane will reveal how they trigger apoptosis.
Our data indicate that dimers do not interact by distinct protein-protein interface, but form disordered clusters to generate pores (Uren et al, eLife, 2017; Uren et al, Philos Trans R Soc Lond B Biol Sci, 2017).
A range of biochemical approaches will examine further how the outer membrane is involved in oligomerisation of dimers.