ArticleScientific reports2016
Methylmercury, an environmental electrophile capable of activation and disruption of the Akt/CREB/Bcl-2 signal transduction pathway in SH-SY5Y cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Elucidating the link between thyroid cancer and mercury exposure: a review and meta-analysis.Environmental science and pollution research international · 2024Pooled it
- Capicua regulates the survival of Cajal-Retzius cells in the postnatal hippocampus.Cell death & disease · 2025Article
- Effects of Environmental Non-Essential Toxic Heavy Metals on Epigenetics During Development.Toxics · 2025Review
- Discovery of a Compound That Inhibits IRE1αACS chemical biology · 2024Article
- Article
- Reduction of Glyoxalase 1 Expression Links Fetal Methylmercury Exposure to Autism Spectrum Disorder Pathogenesis.Toxics · 2024Article
- Early Growth Response Gene-1 Deficiency Interrupts TGFβ1 Signaling Activation and Aggravates Neurodegeneration in Experimental Autoimmune Encephalomyelitis Mice.Neuroscience bulletin · 2024Article
- Elemental biomapping of human tissues suggests toxic metals such as mercury play a role in the pathogenesis of cancer.Frontiers in oncology · 2024Article
- Methylmercury directly modifies the 105th cysteine residue in oncostatin M to promote binding to tumor necrosis factor receptor 3 and inhibit cell growth.Archives of toxicology · 2023Article
- Prenatal low-dose methylmercury exposure causes premature neuronal differentiation and autism-like behaviors in a rodent model.iScience · 2023Article
- Ghrelin attenuates methylmercury-induced oxidative stress in neuronal cells.Molecular neurobiology · 2022Article
- Increased expression of TCF3, transcription factor 3, is a defense response against methylmercury toxicity in mouse neuronal C17.2 cells.Toxicological research · 2021Article
- The fate of methylmercury through the formation of bismethylmercury sulfide as an intermediate in mice.Scientific reports · 2021Article
- The antioxidant role of STAT3 in methylmercury-induced toxicity in mouse hypothalamic neuronal GT1-7 cell line.Free radical biology & medicine · 2021Article
- DNA methyltransferase- and histone deacetylase-mediated epigenetic alterations induced by low-level methylmercury exposure disrupt neuronal development.Archives of toxicology · 2021Article
- Sulfhydryl groups as targets of mercury toxicity.Coordination chemistry reviews · 2020Article
- Redox toxicology of environmental chemicals causing oxidative stress.Redox biology · 2020Review
- Nrf2 Activation and Its Coordination with the Protective Defense Systems in Response to Electrophilic Stress.International journal of molecular sciences · 2020Review
- LncRNA LINC00641 Sponges miR-497-5p to Ameliorate Neural Injury Induced by Anesthesia via Up-Regulating BDNF.Frontiers in molecular neuroscience · 2020Article
- Adaptive Responses to Electrophilic Stress and Reactive Sulfur Species as their Regulator Molecules.Toxicological research · 2019Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylmercury (MeHg) modifies cellular proteins via their thiol groups in a process referred to as "S-mercuration", potentially resulting in modulation of the cellular signal transduction pathway. We examined whether low-dose MeHg could affect Akt signaling involved in cell survival. Exposure of human neuroblastoma SH-SY5Y cells of up to 2 μM MeHg phosphorylated Akt and its downstream signal molecule CREB, presumably due to inactivation of PTEN through S-mercuration. As a result, the anti-apoptotic protein Bcl-2 was up-regulated by MeHg. The activation of Akt/CREB/Bcl-2 signaling mediated by MeHg was, at least in part, linked to cellular defence because either pretreatment with wortmannin to block PI3K/Akt signaling or knockdown of Bcl-2 enhanced MeHg-mediated cytotoxicity. In contrast, increasing concentrations of MeHg disrupted Akt/CREB/Bcl-2 signaling. This phenomenon was attributed to S-mercuration of CREB through Cys286 rather than Akt. These results suggest that although MeHg is an apoptosis-inducing toxicant, this environmental electrophile is able to activate the cell survival signal transduction pathway at lower concentrations prior to apoptotic cell death.
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