ArticleThe Biochemical journal2015
DJ1 represses glycolysis and cell proliferation by transcriptionally up-regulating Pink1.
Article in The Biochemical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Review
- Dopaminergic neuron metabolism: relevance for understanding Parkinson's disease.Metabolomics : Official journal of the Metabolomic Society · 2024Review
- Molecular and Physiological Determinants of Amyotrophic Lateral Sclerosis: What the DJ-1 Protein Teaches Us.International journal of molecular sciences · 2023Review
- Deficiency of Parkinson's Related Protein DJ-1 Alters Cdk5 Signalling and Induces Neuronal Death by Aberrant Cell Cycle Re-entry.Cellular and molecular neurobiology · 2023Article
- PINK1 regulates apoptosis of osteosarcoma as the target gene of cisplatin.Journal of orthopaedic surgery and research · 2023Article
- Exploring the link between Parkinson's disease and type 2 diabetes mellitus in Drosophila.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Metabolic Features of Brain Function with Relevance to Clinical Features of Alzheimer and Parkinson Diseases.Molecules (Basel, Switzerland) · 2022Review
- Parkinson's disease protein PARK7 prevents metabolite and protein damage caused by a glycolytic metabolite.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A High-Throughput Chemical Screen in DJ-1β Mutant Flies Identifies Zaprinast as a Potential Parkinson's Disease Treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Review
- Mitochondrial Metabolism as Target of the Neuroprotective Role of Erythropoietin in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2021Article
- The crosstalk of NAD, ROS and autophagy in cellular health and ageing.Biogerontology · 2020Review
- Genetics of Parkinson's disease: An introspection of its journey towards precision medicine.Neurobiology of disease · 2020Review
- A Novel Pyrazolopyrimidine Ligand of Human PGK1 and Stress Sensor DJ1 Modulates the Shelterin Complex and Telomere Length Regulation.Neoplasia (New York, N.Y.) · 2019Article
- δ-Opioid Receptor Activation Attenuates the Oligomer Formation Induced by Hypoxia and/or α-Synuclein Overexpression/Mutation Through Dual Signaling Pathways.Molecular neurobiology · 2019Article
- Thioredoxin and glutaredoxin regulate metabolism through different multiplex thiol switches.Redox biology · 2019Article
- Reduction of PINK1 or DJ-1 impair mitochondrial motility in neurites and alter ER-mitochondria contacts.Journal of cellular and molecular medicine · 2018Article
- Astroglial DJ-1 over-expression up-regulates proteins involved in redox regulation and is neuroprotective in vivo.Redox biology · 2018Article
- Linking Glycation and Glycosylation With Inflammation and Mitochondrial Dysfunction in Parkinson's Disease.Frontiers in neuroscience · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
DnaJ-1 or hsp40/hdj-1 (DJ1) is a multi-functional protein whose mutations cause autosomal recessive early-onset Parkinson's disease (PD). DJ1 loss of function disrupts mitochondrial function, but the signalling pathway, whereby it interferes with energy metabolism, is unknown. In the present study, we found that mouse embryonic fibroblasts (MEFs) obtained from DJ1-null (dj1-/-) mice showed higher glycolytic rate than those from wild-type (WT) DJ1 (dj1+/+). This effect could be counteracted by the expression of the full-length cDNA encoding the WT DJ1, but not its DJ1-L166P mutant form associated with PD. Loss of DJ1 increased hypoxia-inducible factor-1α (Hif1α) protein abundance and cell proliferation. To understand the molecular mechanism responsible for these effects, we focused on phosphatase and tensin homologue deleted on chromosome 10 (PTEN)-induced protein kinase-1 (Pink1), a PD-associated protein whose loss was recently reported to up-regulate glucose metabolism and to sustain cell proliferation [Requejo-Aguilar et al. (2014) Nat. Commun. 5, 4514]. Noticeably, we found that the alterations in glycolysis, Hif1α and proliferation of DJ1-deficient cells were abrogated by the expression of Pink1. Moreover, we found that loss of DJ1 decreased pink1 mRNA and Pink1 protein levels and that DJ1, by binding with Foxo3a (forkhead box O3a) transcription factor, directly interacted with the pink1 promoter stimulating its transcriptional activity. These results indicate that DJ1 regulates cell metabolism and proliferation through Pink1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.