ArticleNeuromolecular medicine2014
β-Amyloid-evoked apoptotic cell death is mediated through MKK6-p66shc pathway.
Article in Neuromolecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- The Role of the Redox Enzyme p66Shc in Biological Aging of the Lung.Aging and disease · 2024Article
- MAP2K6 remodels chromatin and facilitates reprogramming by activating Gatad2b-phosphorylation dependent heterochromatin loosening.Cell death and differentiation · 2022Article
- Amyloid and Tau Induce Cell Death Independently of TSPO Polymerization and Density Changes.ACS omega · 2021Article
- Resolvin D1 Prevents the Impairment in the Retention Memory and Hippocampal Damage in Rats Fed a Corn Oil-Based High Fat Diet by Upregulation of Nrf2 and Downregulation and Inactivation of pNeurochemical research · 2020Article
- p66Shc activation promotes increased oxidative phosphorylation and renders CNS cells more vulnerable to amyloid beta toxicity.Scientific reports · 2018Review
- New aspects of p66Shc in ischaemia reperfusion injury and other cardiovascular diseases.British journal of pharmacology · 2017Review
- Genetic ablation of the p66Molecular psychiatry · 2017Article
- The carbonic anhydrase inhibitor methazolamide prevents amyloid beta-induced mitochondrial dysfunction and caspase activation protecting neuronal and glial cells in vitro and in the mouse brain.Neurobiology of disease · 2016Article
- p66Shc as a switch in bringing about contrasting responses in cell growth: implications on cell proliferation and apoptosis.Molecular cancer · 2015Review
- TAT-OSBP-1-MKK6(E), a novel TAT-fusion protein with high selectivity for human ovarian cancer, exhibits anti-tumor activity.Medical oncology (Northwood, London, England) · 2015Article
- Ouabain elicits human glioblastoma cells apoptosis by generating reactive oxygen species in ERK-p66SHC-dependent pathway.Molecular and cellular biochemistry · 2015Article
- The toxicity mechanisms of action of Aβ25-35 in isolated rat cardiac myocytes.Molecules (Basel, Switzerland) · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown the involvement of p66shc in mediating apoptosis. Here, we demonstrate the novel mechanism of β-Amyloid-induced toxicity in the mammalian cells. β-Amyloid leads to the phosphorylation of p66shc at the serine 36 residue and activates MKK6, by mediating the phosphorylation at serine 207 residue. Treatment of cells with antioxidants blocks β-Amyloid-induced serine phosphorylation of MKK6, reactive oxygen species (ROS) generation, and hence protected cells against β-Amyloid-induced cell death. Our results indicate that serine phosphorylation of p66shc is carried out by active MKK6. MKK6 knock-down resulted in decreased serine 36 phosphorylation of p66shc. Co-immunoprecipitation results demonstrate a direct physical association between p66shc and WT MKK6, but not with its mutants. Increase in β-Amyloid-induced ROS production was observed in the presence of MKK6 and p66shc, when compared to triple mutant of MKK6 (inactive) and S36 mutant of p66shc. ROS scavengers and knock-down against p66shc, and MKK6 significantly decreased the endogenous level of active p66shc, ROS production, and cell death. Finally, we show that the MKK6-p66shc complex mediates β-Amyloid-evoked apoptotic cell death.
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