ArticleExperimental & molecular medicine2008
Cytosolic accumulation of gammaH2AX is associated with tropomyosin-related kinase A-induced cell death in U2OS cells.
Article in Experimental & molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- H2AX C-Terminal Dipeptide Truncation: A Master Switch of the DNA Damage Response.bioRxiv : the preprint server for biology · 2026Article
- Hepatic Inflammation and Liver Injury in a Model of Bacterial Infection Triggered Acute-on-Chronic Liver Injury.Journal of gastroenterology and hepatology · 2025Article
- Lovastatin-Induced Mitochondrial Oxidative Stress Leads to the Release of mtDNA to Promote Apoptosis by Activating cGAS-STING Pathway in Human Colorectal Cancer Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Pharmacological Ascorbate Elicits Anti-Cancer Activities against Non-Small Cell Lung Cancer through Hydrogen-Peroxide-Induced-DNA-Damage.Antioxidants (Basel, Switzerland) · 2023Article
- dSTORM microscopy evidences in HeLa cells clustered and scattered γH2AX nanofoci sensitive to ATM, DNA-PK, and ATR kinase inhibitors.Molecular and cellular biochemistry · 2020Article
- Article
- Effectiveness of a Fractionated Therapy Scheme in Tumor Treating Fields Therapy.Technology in cancer research & treatment · 2019Article
- Cross-talk between androgen receptor and nerve growth factor receptor in prostate cancer cells: implications for a new therapeutic approach.Cell death discovery · 2018Article
- LMTK3 confers chemo-resistance in breast cancer.Oncogene · 2018Article
- Low-density Lipoprotein Receptor-related Proteins in a Novel Mechanism of Axon Guidance and Peripheral Nerve Regeneration.The Journal of biological chemistry · 2016Article
- Blocking Nerve Growth Factor Signaling Reduces the Neural Invasion Potential of Pancreatic Cancer Cells.PloS one · 2016Article
- Cross-talk between androgen receptor/filamin A and TrkA regulates neurite outgrowth in PC12 cells.Molecular biology of the cell · 2015Article
- Induction of neurite outgrowth in PC12 cells treated with temperature-controlled repeated thermal stimulation.PloS one · 2015Article
- The role of TRKA signaling in IL-10 production by apoptotic tumor cell-activated macrophages.Oncogene · 2013Article
- Proteomic analysis of novel targets associated with TrkA-mediated tyrosine phosphorylation signaling pathways in SK-N-MC neuroblastoma cells.Proteomics · 2013Article
- Transcription of the protein kinase C-delta gene is activated by JNK through c-Jun and ATF2 in response to the anticancer agent doxorubicin.Experimental & molecular medicine · 2008Article
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
Tropomyosin-related kinase A (TrkA) plays an important role in cell survival, differentiation, and apoptosis in various neuronal and nonneuronal cell types. Here we show that TrkA overexpression by the Tet-On system mimics NGF-mediated activation pathways in the absence of nerve growth factor (NGF) stimulation in U2OS cells. In addition, p53 upregulation upon DNA damage was inhibited by TrkA, and p21 was upregulated by TrkA in a p53-independent manner. TrkA overexpression caused cell death by interrupting cell cycle progression, and TrkA-induced cell death was diminished in the presence of its specific inhibitor GW441756. Interestingly, TrkA-mediated cell death was strongly related to gammaH2AX production and poly (ADP-ribose) polymerase cleavage in the absence of DNA damage inducer. In this study, we also reveal that gammaH2AX production by TrkA is blocked by TrkA kinase inhibitors K-252a and GW441756, and it is also significantly inhibited by JNK inhibitor SP600125. Moreover, reduction of cell viability by TrkA was strongly suppressed by SP600125 treatment, suggesting a critical role of JNK in TrkA-induced cell death. We also found that gammaH2AX and TrkA were colocalized in cytosol in the absence of DNA damage, and the nuclear localization of gammaH2AX induced by DNA damage was partly altered to cytosol by TrkA overexpression. Our results suggest that the abnormal cytosolic accumulation of gammaH2AX is implicated in TrkA-induced cell death in the absence of DNA damage.
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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.