Some experiments were aimed at finding how SOD1 becomes pro-apoptotic (promoting programmed cell death) due to the fact that healthy SOD1 are against programmed cell death (Pasinelli et al. 2004). The pro-apoptotic characteristic of mutant SOD1 is demonstrated in vivo and in vitro. The mitochondria inside cells firmly control apoptosis
, and the mutant SOD1 that aggregates inside mitochondria triggers the programmed cell death
of motor neurons (Pasinelli et al. 2004). One experiment studied proteins that interact with mutant SOD1, specifically Bcl-2 which is anti-apoptotic, in order to explain the apoptotic nature of mutant SOD1 (Pasinelli et al. 2004). The methods that were used involve in vitro approaches and Western blot analysis. The outcomes were that mutant SOD1 and Bcl-2 interact with each other in vivo in the spinal cord
, and they both together are pro-apoptotic (Pasinelli et al. 2004). In other words, Bcl-2 was an anti-apoptotic protein when standing alone, and when it directly interacted with mutant SOD1, the protein and the gene convert to pro-apoptosis, or in support of cell death; this could be due to a conformational change in Bcl-2.