ArticleCell death and differentiation2016
FAF1 mediates regulated necrosis through PARP1 activation upon oxidative stress leading to dopaminergic neurodegeneration.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
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- Tipping the PARylation scale: Dysregulation of PAR signaling in Huntington and neurodegenerative diseases.Journal of Huntington's disease · 2025Review
- Oxidative stress and its related epigenetic modifications in vascular calcification: mechanisms and advances.Frontiers in cardiovascular medicine · 2025Review
- Sumoylation of SAP130 regulates its interaction with FAF1 as well as its protein stability and transcriptional repressor function.BMC molecular and cell biology · 2024Article
- Engineered Selenium/Human Serum Albumin Nanoparticles for Efficient Targeted Treatment of Parkinson's Disease via Oral Gavage.ACS nano · 2023Article
- Substance abuse and neurodegenerative diseases: focus on ferroptosis.Archives of toxicology · 2023Review
- Non-coding RNAs in necroptosis, pyroptosis and ferroptosis in cancer metastasis.Cell death discovery · 2021Review
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- PARP overactivation in neurological disorders.Molecular biology reports · 2021Review
- Fas-Associated Factor 1 Promotes Hepatic Insulin Resistance via JNK Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
- A novel function of FAF1, which induces dopaminergic neuronal death through cell-to-cell transmission.Cell communication and signaling : CCS · 2020Article
- FAF1 mediates necrosis through JNK1-mediated mitochondrial dysfunction leading to retinal degeneration in the ganglion cell layer upon ischemic insult.Cell communication and signaling : CCS · 2018Article
- Spatiotemporal Protein Atlas of Cell Death-Related Molecules in the Rat MCAO Stroke Model.Experimental neurobiology · 2018Article
- Cell Death Pathways: a Novel Therapeutic Approach for Neuroscientists.Molecular neurobiology · 2018Review
- Loss of Drosha underlies dopaminergic neuron toxicity in models of Parkinson's disease.Cell death & disease · 2018Article
- Curcumin pretreatment prevents hydrogen peroxide-induced oxidative stress through enhanced mitochondrial function and deactivation of Akt/Erk signaling pathways in rat bone marrow mesenchymal stem cells.Molecular and cellular biochemistry · 2018Article
- Fas-associated factor 1 inhibits tumor growth by suppressing Helicobacter pylori-induced activation of NF-κB signaling in human gastric carcinoma.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cumulative damage caused by oxidative stress results in diverse pathological conditions. Therefore, elucidating the molecular mechanisms underlying cell death following oxidative stress is important. Here, we describe a novel role for Fas-associated factor 1 (FAF1) as a crucial regulator of necrotic cell death elicited by hydrogen peroxide. Upon oxidative insult, FAF1 translocated from the cytoplasm to the nucleus and promoted the catalytic activation of poly(ADP-ribose) polymerase 1 (PARP1) through physical interaction. Moreover, FAF1 depletion prevented PARP1-linked downstream events involved in the triggering of cell death, including energetic collapse, mitochondrial depolarization and nuclear translocation of apoptosis-inducing factor (AIF), implying that FAF1 has a key role in PARP1-dependent necrosis in response to oxidative stress. We further investigated whether FAF1 might contribute to the pathogenesis of Parkinson's disease through excessive PARP1 activation. Indeed, the overexpression of FAF1 using a recombinant adeno-associated virus system in the mouse ventral midbrain promoted PARP1 activation and dopaminergic neurodegeneration in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. Collectively, our data demonstrate the presence of an FAF1-PARP1 axis that is involved in oxidative stress-induced necrosis and in the pathology of Parkinson's disease.
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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.