ArticleNeurobiology of disease2009
Oxidative damage to the promoter region of SQSTM1/p62 is common to neurodegenerative disease.
Article in Neurobiology of disease, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 93 citations in OpenAlex.
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- Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer's Disease.Biomedicines · 2022Review
- The spectrum of neurodevelopmental, neuromuscular and neurodegenerative disorders due to defective autophagy.Autophagy · 2022Article
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- Expression Pattern of p62 in Primary Age-Related Tauopathy: Staging of p62 in PART.Frontiers in aging neuroscience · 2022Article
- Macroautophagy and aging: The impact of cellular recycling on health and longevity.Molecular aspects of medicine · 2021Review
- A neuropathological cell model derived from Niemann-Pick disease type C patient-specific iPSCs shows disruption of the p62/SQSTM1-KEAP1-NRF2 Axis and impaired formation of neuronal networks.Molecular genetics and metabolism reports · 2021Article
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- Autophagy and disease: unanswered questions.Cell death and differentiation · 2020Review
- Germacrone Regulates HBXIP-Mediated Cell Cycle, Apoptosis and Promotes the Formation of Autophagosomes to Inhibit the Proliferation of Gastric Cancer Cells.Frontiers in oncology · 2020Article
- Gap Junction Intercellular Communication Negatively Regulates Cadmium-Induced Autophagy and Inhibition of Autophagic Flux in Buffalo Rat Liver 3A Cells.Frontiers in pharmacology · 2020Article
- Autophagy, Cellular Aging and Age-related Human Diseases.Experimental neurobiology · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Recently we reported that declined SQSTM1/p62 expression in Alzheimer disease brain was age-correlated with oxidative damage to the p62 promoter. The objective of this study was to examine whether oxidative damage to the p62 promoter is common to DNA recovered from brain of individuals with neurodegenerative disease. Increased 8-OHdG staining was observed in brain sections from Alzheimer's disease (AD), Parkinson disease (PD), Huntington disease (HD), Frontotemporal dementia (FTD), and Pick's disease compared to control subjects. In parallel, the p62 promoter exhibited elevated oxidative damage in samples from various diseases compared to normal brain, and damage was negatively correlated with p62 expression in FTD samples. Oxidative damage to the p62 promoter induced by H2O2 treatment decreased its transcriptional activity. In keeping with this observation, the transcriptional activity of a Sp-1 element deletion mutant displayed reduced stimulus-induced activity. These findings reveal that oxidative damage to the p62 promoter decreased its transcriptional activity and might therefore account for decreased expression of p62. Altogether these results suggest that pharmacological means to increase p62 expression may be beneficial in delaying the onset of neurodegeneration.
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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.