When you look at what Prana already have demonstrated, up regulation of DJ-1, we have already seen mitochondria effects. There has been quite a lot of independent research on DJ-1. examples:
[Surprisingly, up-regulation of
DJ-1 can ameliorate
pink1, but not
parkin, mutants in
Drosophila; cysteine C104 (analogous to C106 in human) is critical for this rescue, implicating the oxidative functions of DJ-1 in this property. These results suggest that
DJ-1 is important for proper mitochondrial function and acts downstream of, or in parallel to,
pink1. These findings link
DJ-1,
pink1, and
parkin to mitochondrial integrity and provide the foundation for therapeutics that link bioenergetics and parkinsonism.]
http://www.pnas.org/content/107/21/9747
[Here we report that at basal conditions DJ-1 is present mostly in the cytoplasm and to a lesser extent in mitochondria and nucleus of dopaminergic neuroblastoma SK-N-BE(2)C cells. Upon oxidant challenge, more DJ-1 translocates to mitochondria within 3 hours and subsequently to the nucleus by 12 hours. The predominant DJ-1 species in both mitochondria and nucleus is a dimer believed to be the functional form.]
[Compared with 30% protection against oxidant induced cell death in wild-type DJ-1-transfected cells, mitochondrial targeting of DJ-1 provided a significantly stronger (55%) cytoprotection based on LDH release.]
[Similarly,
DJ-1 null mice are more vulnerable to MPTP than their wild-type littermates (
Kim et al. 2005)]
[Second, DJ-1 modulates transcription through interacting with DJ-1 binding protein (DJBP) (
Niki et al. 2003)]
[ Third, DJ-1 is a regulatory subunit (RS) of an RNA-binding protein (
Hod et al. 1999). ]
[Fourth, DJ-1 may have chaperone activity, preventing heat-induced aggregation of substrate proteins (
Lee et al. 2003) including α-synuclein (
Shendelman et al. 2004;
Zhou and Freed 2005) ]
[Fifth, catalytic activities for DJ-1 have been suggested, including a cysteine protease function (
Honbou et al. 2003;
Olzmann et al. 2003), but not confirmed (
Lee et al. 2003;
Shendelman et al. 2004;
Wilson et al. 2003). It is conceivable that many if not all of these functions relate to the pathogenetic role of DJ-1 in PD.]
[ These findings suggest that mitochondrial localization confers DJ-1 superior neuroprotective function against oxidative stress than cytosolic or nuclear localization.]
[In conclusion, the present observations highlight the cytoprotective effect of DJ-1 present as a dimer in the outer membrane of mitochondria without necessarily being oxidized at its cysteine residues. Elucidating the processes that lead from its mitochondrial translocation to cell survival requires additional investigations.]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752655/
