ArticleCell death & disease2020
Parp3 promotes astrocytic differentiation through a tight regulation of Nox4-induced ROS and mTorc2 activation.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Rictor/mTORC2 signaling pathway protects endogenous neural stem cells to promote recovery after spinal cord injury.Neural regeneration research · 2026Article
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Targeting MARylation and DePARylation in Cancer Therapy: New Promising Therapeutic Opportunities.Cancers · 2025Review
- Article
- Early transcriptional responses reveal cell type-specific vulnerability and neuroprotective mechanisms in the neonatal ischemic hippocampus.Acta neuropathologica communications · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Hand Osteoarthritis: Molecular Mechanisms, Randomized Controlled Trials, and the Future of Targeted Treatment.International journal of molecular sciences · 2025Review
- Parp3 assists muscle function and skeletal muscle differentiation by selectively adjusting H3K27me3 enrichment.iScience · 2025Article
- Blood-testis barrier: a review on regulators in maintaining cell junction integrity between Sertoli cells.Cell and tissue research · 2024Review
- Dysregulation of DNA repair genes in Fuchs endothelial corneal dystrophy.Experimental eye research · 2023Article
- Prognostic analysis of patients with breast cancer based on tumor mutational burden and DNA damage repair genes.Frontiers in oncology · 2023Article
- PARP12 is required for mitochondrial function maintenance in thermogenic adipocytes.Adipocyte · 2022Article
- Role of NADPH Oxidases in Blood-Brain Barrier Disruption and Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2022Review
- PARP3 supervises G9a-mediated repression of adhesion and hypoxia-responsive genes in glioblastoma cells.Scientific reports · 2022Article
- Dysregulation of mTOR Signaling after Brain Ischemia.International journal of molecular sciences · 2022Review
- Nicotinamide-riboside shifts the differentiation of human primary white adipocytes to beige adipocytes impacting substrate preference and uncoupling respiration through SIRT1 activation and mitochondria-derived reactive species production.Frontiers in cell and developmental biology · 2022Article
- NADPH Oxidases: Redox Regulators of Stem Cell Fate and Function.Antioxidants (Basel, Switzerland) · 2021Review
- Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parp3 is a member of the Poly(ADP-ribose) polymerase (Parp) family that has been characterized for its functions in strand break repair, chromosomal rearrangements, mitotic segregation and tumor aggressiveness. Yet its physiological implications remain unknown. Here we report a central function of Parp3 in the regulation of redox homeostasis in continuous neurogenesis in mice. We show that the absence of Parp3 provokes Nox4-induced oxidative stress and defective mTorc2 activation leading to inefficient differentiation of post-natal neural stem/progenitor cells to astrocytes. The accumulation of ROS contributes to the decreased activity of mTorc2 as a result of an oxidation-induced and Fbxw7-mediated ubiquitination and degradation of Rictor. In vivo, mTorc2 signaling is compromised in the striatum of naïve post-natal Parp3-deficient mice and 6 h after acute hypoxia-ischemia. These findings reveal a physiological function of Parp3 in the tight regulation of striatal oxidative stress and mTorc2 during astrocytic differentiation and in the acute phase of hypoxia-ischemia.
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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 Socratic graph.