DJ-1 protects cell death from a mitochondrial oxidative stress due to GBA1 deficiency.
Younwoo NamJiyeon NaShi-Xun MaHaeun ParkHyeonwoo ParkEunmin LeeHyerynn KimSang-Min JangHan Seok KoSangjune KimPublished in: Genes & genomics (2024)
Taken together, our results suggest that DJ-1 upregulation due to GBA1 deficiency has a protective role against oxidative stress. It may be supposed that mutations or malfunctions in the DJ-1 protein may have disadvantages in the survival of dopaminergic neurons in the brains of patients harboring GBA1 mutations.
Keyphrases
- oxidative stress
- cell death
- end stage renal disease
- newly diagnosed
- dna damage
- chronic kidney disease
- ejection fraction
- ischemia reperfusion injury
- diabetic rats
- peritoneal dialysis
- prognostic factors
- cell proliferation
- induced apoptosis
- replacement therapy
- patient reported outcomes
- long non coding rna
- free survival
- small molecule
- heat shock
- cell cycle arrest
- smoking cessation
- heat shock protein