Growth death rate interactions

Bax is another member of this family of proteins that forms both homodimers and heterodimers with Bcl-2. When overexpressed, Bax has been shown to accelerate cell death induced by growth factor deprivation in an IL-3-dependent cell line (Oltvai et al., 1993). However, overexpression of Bax is not sufficient to trigger apoptosis (Korsmeyer et al., 1993). Expression of Bax is more widespread than that of Bcl-2 and appears to be associated with cells that have a high rate of spontaneous or inducible apoptosis (Krajewski et al., 1994). It has been shown that Bax interacts with Bcl-2 via the BHl and BH2 domains. Evidence that the protection from apoptosis afforded by Bcl-2 is mediated via its heterodimers with Bax rather than Bcl-2 homodimers was obtained from experiments involving mutations of Bcl-2 that prevent the former, but not the latter (Yin et al.,... 

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