Calpain-induced Bax-cleavage product is a more potent inducer of apoptotic cell death than wild-type Bax

Inhibition of N-(4-hydroxyphenyl)retinamide-Induced Apoptosis in Breast Cancer Cells by Galectin-3

“…It has been reported recently that p21 Bax can be cleaved to generate p18 Bax during the apoptotic processes by the caspase-activated protease calpain. 35,36 The p18 protein, which lacks NH 2 -terminal amino acids 1 to 28 (tBax 29 ), functions as a more potent inducer of apoptosis than intact p21 Bax. 37,38 At least part of the mechanism of its action involves decreased ability of Bcl-x L to rescue cells in which tBax29 is formed in spite of the complex formation between the two.…”

Autophagy, Apoptosis, Mitoptosis and Necrosis: Interdependence Between Those Pathways and Effects on Cancer

“…Activated calpains, for example, cleave the anti-apoptotic Bcl-XL and Bax, as well as caspase-7, -8 and -9. It is however not clear if this cleavage inhibits or stimulates caspase activity (Chua et al 2000;Lee et al 2006;Toyota et al 2003;.…”

Multistep and multitask Bax activation

“…Among the pro-apoptotic responses, calpains have been shown to proteolytically activate Bax by cleaving its N-terminal region (Gao and Dou, 2000). This truncated Bax is highly active, possibly because a negative regulation signal has been removed (Toyota et al, 2003). In addition, calpain were also shown to cleave Bid to a cleavage site distinct from caspase 8 (Chen et al, 2001); this calpain-dependent t-Bid shares similar pro-apoptotic activity with caspase 8-cleaved t-Bid (Mandic et al, 2002), including Bax recruitment.…”