ArticleGene2011
Functional activity of the novel Alzheimer's amyloid β-peptide interacting domain (AβID) in the APP and BACE1 promoter sequences and implications in activating apoptotic genes and in amyloidogenesis.
Article in Gene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 73 citations in OpenAlex.
- MicroRNA-181 influences Alzheimer's risk by regulating neprilysin and microtubule-associated tau pathways, offering a novel target.bioRxiv : the preprint server for biology · 2026Article
- The mRNA Expression Levels of General Transcription Factors Altered in Alzheimer Cases Possibly Due to Amyloid Beta 1-42 Exposure.Noro psikiyatri arsivi · 2026Article
- Nuclear pore dysfunction and disease: a complex opportunity.Nucleus (Austin, Tex.) · 2024Review
- Modeling genotype-protein interaction and correlation for Alzheimer's disease: a multi-omics imaging genetics study.Briefings in bioinformatics · 2024Article
- Review
- Could Amyloid-β 1-42 or α-Synuclein Interact Directly with Mitochondrial DNA? A Hypothesis.ACS chemical neuroscience · 2022Review
- Effects of microRNA-298 on APP and BACE1 translation differ according to cell type and 3'-UTR variation.Scientific reports · 2022Article
- Alzheimer's Disease: A Molecular View of β-Amyloid Induced Morbific Events.Biomedicines · 2021Review
- Looking at Alzheimer's Disease Pathogenesis from the Nuclear Side.Biomolecules · 2021Review
- Gene biomarker discovery at different stages of Alzheimer using gene co-expression network approach.Scientific reports · 2020Article
- Lithium alters expression of RNAs in a type-specific manner in differentiated human neuroblastoma neuronal cultures, including specific genes involved in Alzheimer's disease.Scientific reports · 2019Article
- Icariin Ameliorates Amyloid Pathologies by Maintaining Homeostasis of Autophagic Systems in AβNeurochemical research · 2019Article
- Powering Amyloid Beta Degrading Enzymes: A Possible Therapy for Alzheimer's Disease.Neurochemical research · 2019Review
- Tyrosine Rotamer States in Beta Amyloid: Signatures of Aggregation and Fibrillation.ACS omega · 2018Article
- The Transcriptional Regulatory Properties of Amyloid Beta 1-42 may Include Regulation of Genes Related to Neurodegeneration.Neuromolecular medicine · 2018Article
- The transcription factor XBP1 in memory and cognition: Implications in Alzheimer disease.Molecular medicine (Cambridge, Mass.) · 2017Article
- NFATc2 Modulates Microglial Activation in the AβPP/PS1 Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2017Article
- Aberrant Co-localization of Synaptic Proteins Promoted by Alzheimer's Disease Amyloid-β Peptides: Protective Effect of Human Serum Albumin.Journal of Alzheimer's disease : JAD · 2017Article
- Calcium-Sensing Receptors of Human Neural Cells Play Crucial Roles in Alzheimer's Disease.Frontiers in physiology · 2016Review
- APP Causes Hyperexcitability in Fragile X Mice.Frontiers in molecular neuroscience · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Amyloid-β peptide (Aβ) plaque in the brain is the primary (post mortem) diagnostic criterion of Alzheimer's disease (AD). The physiological role(s) of Aβ are poorly understood. We have previously determined an Aβ interacting domain (AβID) in the promoters of AD-associated genes (Maloney and Lahiri, 2011. Gene. 15,doi:10.1016/j.gene.2011.06.004. epub ahead of print.). This AβID interacts in a DNA sequence-specific manner with Aβ. We now demonstrate novel Aβ activity as a possible transcription factor. Herein, we detected Aβ-chromatin interaction in cell culture by ChIP assay. We observed that human neuroblastoma (SK-N-SH) cells treated with FITC conjugated Aβ1-40 localized Aβ to the nucleus in the presence of H2O2-mediated oxidative stress. Furthermore, primary rat fetal cerebrocortical cultures were transfected with APP and BACE1 promoter-luciferase fusions, and rat PC12 cultures were transfected with polymorphic APP promoter-CAT fusion clones. Transfected cells were treated with different Aβ peptides and/or H2O2. Aβ treatment of cell cultures produced a DNA sequence-specific response in cells transfected with polymorphic APP clones. Our results suggest the Aβ peptide may regulate its own production through feedback on its precursor protein and BACE1, leading to amyloidogenesis in AD.
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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.