ArticleJournal of cell science2012
GRIM-19-mediated translocation of STAT3 to mitochondria is necessary for TNF-induced necroptosis.
Article in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 60 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 100 citations in OpenAlex.
- Dynamics in Redox-Active Molecules Following Ischemic Preconditioning in the Brain.Neurology international · 2024Article
- STAT3 protects dopaminergic neurons against degeneration in animal model of Parkinson's disease.Brain research · 2024Article
- TNFα-Induced Oxidative Stress and Mitochondrial Dysfunction Alter Hypothalamic Neurogenesis and Promote Appetite Versus Satiety Neuropeptide Expression in Mice.Brain sciences · 2022Article
- Glial Purinergic Signaling-Mediated Oxidative Stress (GPOS) in Neuropsychiatric Disorders.Oxidative medicine and cellular longevity · 2022Review
- Age-Dependent Decline in Neuron Growth Potential and Mitochondria Functions in Cortical Neurons.Cells · 2021Article
- Necroptosis and RhoA/ROCK pathways: molecular targets of Nesfatin-1 in cardioprotection against myocardial ischemia/reperfusion injury in a rat model.Molecular biology reports · 2021Article
- Review
- Caspase-Independent Regulated Necrosis Pathways as Potential Targets in Cancer Management.Frontiers in oncology · 2020Review
- A Potent and Selective Small-Molecule Degrader of STAT3 Achieves Complete Tumor Regression In Vivo.Cancer cell · 2019Article
- Targeting necroptotic cell death pathway by high-intensity interval training (HIIT) decreases development of post-ischemic adverse remodelling after myocardial ischemia / reperfusion injury.Journal of cell communication and signaling · 2019Article
- Redox-Related Neuronal Death and Crosstalk as Drug Targets: Focus on Epilepsy.Frontiers in neuroscience · 2019Review
- STAT3-activated CD36 facilitates fatty acid uptake in chronic lymphocytic leukemia cells.Oncotarget · 2018Article
- Essential role of mitochondrial Stat3 in p38Scientific reports · 2017Article
- RIP4 inhibits STAT3 signaling to sustain lung adenocarcinoma differentiation.Cell death and differentiation · 2017Article
- High fat diet-induced obesity increases myocardial injury and alters cardiac STAT3 signaling in mice after polymicrobial sepsis.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Homocysteine induces mitochondrial dysfunction involving the crosstalk between oxidative stress and mitochondrial pSTAT3 in rat ischemic brain.Scientific reports · 2017Article
- Biogenic selenium nanoparticles induce ROS-mediated necroptosis in PC-3 cancer cells through TNF activation.Journal of nanobiotechnology · 2017Article
- Death receptor 3 mediates necroptotic cell death.Cellular and molecular life sciences : CMLS · 2017Article
- FGFR4 polymorphic alleles modulate mitochondrial respiration: A novel target for somatostatin analog action in pituitary tumors.Oncotarget · 2017Article
- GRIM-19 Restricts HCV Replication by Attenuating Intracellular Lipid Accumulation.Frontiers in microbiology · 2017Article
Corrections and comments
- Expression of concern · 2016-02-15Concerns/Issues about Image · Investigation by Company/Institution · Investigation by Journal/Publisher · Objections by Third Party · · This EoC is upgraded by PMID: 27369362, citing Misconduct by John G Pastorino;
- Retraction · 2016-07-01Duplication of/in Image · Falsification/Fabrication of Data · Investigation by Company/Institution · Investigation by Journal/Publisher · Investigation by ORI · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Objections by Third Party · Upgrade/Update of Prior Notice(s) · · Misconduct by John G Pastorino; Expression of Concern at PMID: 26905967 ;
- Commented on by
- Commented on by
- Expression of concern
- Retracted
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Tumor necrosis factor (TNF) can induce necroptosis, wherein inhibition of caspase activity prevents apoptosis but initiates an alternative programmed necrosis. The activity of receptor-interacting serine/threonine-protein kinase 1 (RIPK-1) is required for necroptosis to proceed, with suppression of RIPK-1 expression or inhibition of RIPK-1 activity with necrostatin-1 preventing TNF-induced necroptosis. Downstream from the TNF receptor, the generation of reactive oxygen species at the mitochondria has been identified as necessary for the execution of necroptosis; with antioxidants and inhibitors of mitochondrial complex I preventing TNF-induced cytotoxicity. However, components of the signaling pathway that lie between activated RIPK-1 and the mitochondria are unknown. In the study reported here we demonstrate that during TNF-induced necroptosis, STAT3 is phosphorylated on serine 727, which is dependent on RIPK-1 expression or activity. The phosphorylation of STAT3 induces interaction with GRIM-19, a subunit of mitochondrial complex I, with a resultant translocation of STAT3 to the mitochondria, where it induces an increase in reactive oxygen species production and cell death.
Indexed as
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What OpenQuestion holds
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.