ArticleJournal of Alzheimer's disease : JAD2016
Gene Expression of Quaking in Sporadic Alzheimer's Disease Patients is Both Upregulated and Related to Expression Levels of Genes Involved in Amyloid Plaque and Neurofibrillary Tangle Formation.
Article in Journal of Alzheimer's disease : JAD, 2016. 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, 18 citations in OpenAlex.
- Allele-specific splicing modulates protein isoforms and Alzheimer's risk.bioRxiv : the preprint server for biology · 2026Article
- Microglia and Astrocytes in Alzheimer's Disease: Significance and Summary of Recent Advances.Aging and disease · 2024Review
- RNA binding proteins in cardiovascular development and disease.Current topics in developmental biology · 2024Article
- The multifaceted role of quaking protein in neuropsychiatric disorders and tumor progression.Frontiers in neuroscience · 2024Review
- RNA-Binding Proteins in Bladder Cancer.Cancers · 2023Review
- Review
- MicroRNA and mRNA profiling of cerebral cortex in a transgenic mouse model of Alzheimer's disease by RNA sequencing.Neural regeneration research · 2021Article
- Review
- The Emerging Roles of the RNA Binding Protein QKI in Cardiovascular Development and Function.Frontiers in cell and developmental biology · 2021Review
- Amyloid precursor protein glycosylation is altered in the brain of patients with Alzheimer's disease.Alzheimer's research & therapy · 2020Article
- Accelerated loss of hypoxia response in zebrafish with familial Alzheimer's disease-like mutation of presenilin 1.Human molecular genetics · 2020Article
- Transcriptomic and Network Analysis Identifies Shared and Unique Pathways across Dementia Spectrum Disorders.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Quaking (QKI) is a gene exclusively expressed within glial cells. QKI has previously been implicated in various neurological disorders and diseases, including Alzheimer's disease (AD), a condition for which increasing evidence suggests a central role of glia cells. The objective of the present study was to investigate the expression levels of QKI and three QKI isoforms (QKI5, QKI6, and QKI7) in AD. Genes that have previously been related to the ontogeny and progression of AD, specifically APP, PSEN1, PSEN2, and MAPT, were also investigated. A real-time PCR assay of 123 samples from human postmortem sporadic AD patients and control brains was performed. The expression values were analyzed with an analysis of covariance model and subsequent multiple regressions to explore the possibility of related expression values between QKI, QKI isoforms, and AD-related genes. Further, the sequences of AD-related genes were analyzed for the presence of QKI binding domains. QKI and all measured QKI isoforms were found to be significantly upregulated in AD samples, relative to control samples. However, APP, PSEN1, PSEN2, and MAPT were not found to be significantly different. QKI and QKI isoforms were found to be predictive for the variance of APP, PSEN1, PSEN2, and MAPT, and putative QKI binding sites suggests an interaction with QKI. Overall, these results implicate a possible role of QKI in AD, although the exact mechanism by which this occurs remains to be uncovered.
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