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Background DJ-1 is a protein in association with Parkinson’s disease (PD) and cancers. DJ-1 has been reported to exhibit both cytoplasmic and nuclear distribution (Bonifati et al., Science, 2003; Nagakubo et al., BBRC, 1997). It functions in multiple pathways to affect cell survival. It suppresses the JNK signaling pathway in cytoplasma (Mo et al., Cell Death Differ, 2008) and interacts with Daxx and sequesters it within the nucleus, preventing the initiation of apoptotic signaling (Junn et al., PNAS, 2005). In contrast to its functions in cell survival, deletions or loss of function point mutations in DJ-1 are reported to be responsible for recessive early-onset Parkinson’s disease (PD) (Bonifati et al., Science, 2003). The most commonly studied PD-associated mutant, L166P, is reported to be unstable and to mislocalize to the mitochondria, leading to a loss of the cytoplasmic function of DJ-1 (Bonifati et al., Science, 2003). Although lines of evidence suggest that a high expression of DJ-1 enhances cell survival and loss of DJ-1 function is associated with PD, the detailed mechanisms are still not fully understood.

The role of DJ-1 in anti-apoptosis