ArticleCell death and differentiation2012
The caspase 6 derived N-terminal fragment of DJ-1 promotes apoptosis via increased ROS production.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- DNA Methyltransferase 1 Is Dysregulated in Parkinson's Disease via Mediation of miR-17.Molecular neurobiology · 2021Article
- Tri-arginine exosite patch of caspase-6 recruits substrates for hydrolysis.The Journal of biological chemistry · 2019Article
- Expression of genes that encode cellular oxidant/antioxidant systems are affected by heat stress.Molecular biology reports · 2018Article
- ATP-competitive Plk1 inhibitors induce caspase 3-mediated Plk1 cleavage and activation in hematopoietic cell lines.Oncotarget · 2018Article
- Gene Expression Profiling of Cutaneous Injured and Non-Injured Nociceptors in SNI Animal Model of Neuropathic Pain.Scientific reports · 2017Article
- Atractylenolide-I Protects Human SH-SY5Y Cells from 1-Methyl-4-Phenylpyridinium-Induced Apoptotic Cell Death.International journal of molecular sciences · 2017Article
- Essential control of mitochondrial morphology and function by chaperone-mediated autophagy through degradation of PARK7.Autophagy · 2016Article
- Quantitative MS-based enzymology of caspases reveals distinct protein substrate specificities, hierarchies, and cellular roles.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- TAp73 promotes anabolism.Oncotarget · 2014Article
- Cerebrospinal fluid tau cleaved by caspase-6 reflects brain levels and cognition in aging and Alzheimer disease.Journal of neuropathology and experimental neurology · 2013Article
- DJ-1-dependent regulation of oxidative stress in the retinal pigment epithelium (RPE).PloS one · 2013Article
- Simalikalactone E (SkE), a new weapon in the armamentarium of drugs targeting cancers that exhibit constitutive activation of the ERK pathway.Oncotarget · 2012Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In pathological conditions, the amount of DJ-1 determines whether a cell can survive or engage a cell death program. This is exemplified in epithelial cancers, in which DJ-1 expression is increased, while autosomal recessive early onset Parkinson's disease mutations of DJ-1 generally lead to decreased stability and expression of the protein. We have shown previously that DJ-1 is cleaved by caspase-6 during induction of apoptosis. We demonstrate here that the N-terminal cleaved fragment of DJ-1 (DJ-1 Nt) is specifically expressed in the nucleus and promotes apoptosis in SH-SY5Y neuroblastoma cell lines. In addition, overexpression of DJ-1 Nt in different cell lines leads to a loss of clonogenic potential and sensitizes to staurosporin and 1-methyl-4-phenylpyridinium (MPP+)-mediated caspase activation and apoptosis. Importantly, inhibition of endogenous DJ-1 expression with sh-RNA or DJ-1 deficiency mimics the effect of DJ-1 Nt on cell growth and apoptosis. Moreover, overexpression of DJ-1 Nt increases reactive oxygen species (ROS) production, and sensitizes to MPP+-mediated apoptosis and DJ-1 oxidation. Finally, specific exclusion of DJ-1 Nt from the nucleus abrogates its pro-apoptotic effect. Taken together, our findings identify an original pathway by which generation of a nuclear fragment of DJ-1 through caspase 6-mediated cleavage induces ROS-dependent amplification of apoptosis.
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