ArticleNeuroscience letters2010
APP(DeltaNL695) expression in murine tissue downregulates CNBP expression.
Article in Neuroscience letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 13 citations in OpenAlex.
- The Proteome Profile of Olfactory Ecto-Mesenchymal Stem Cells-Derived from Patients with Familial Alzheimer's Disease Reveals New Insights for AD Study.International journal of molecular sciences · 2023Article
- Cellular nucleic acid-binding protein is essential for type I interferon-mediated immunity to RNA virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- CNBP controls IL-12 gene transcription and Th1 immunity.The Journal of experimental medicine · 2018Article
- CNBP acts as a key transcriptional regulator of sustained expression of interleukin-6.Nucleic acids research · 2017Article
- Bridging integrator 1 (BIN1) protein expression increases in the Alzheimer's disease brain and correlates with neurofibrillary tangle pathology.Journal of Alzheimer's disease : JAD · 2014Article
- Beyond the binding site: in vivo identification of tbx2, smarca5 and wnt5b as molecular targets of CNBP during embryonic development.PloS one · 2013Article
- Yeast Gis2 and its human ortholog CNBP are novel components of stress-induced RNP granules.PloS one · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The cellular nucleic acid binding protein (CNBP) is a ubiquitously expressed protein involved in regulation of transcription and translation. CNBP, and its encoding gene ZNF9, have been shown to be involved in type 2 myotonic dystrophy. Both Alzheimer's disease (AD) and sporadic inclusion body myositis (sIBM) are age-related degenerative diseases associated with the accumulation of beta-amyloid. Overexpression of amyloid precursor protein (APP) in mice has been used to generate models of both diseases. We show here that overexpression of APP in skeletal muscle from a mouse model of sIBM reduces the expression of CNBP significantly. We examined CNBP expression in a brain-specific APP-overexpressing strain, and a whole body APP knock-in strain, and found that there was a reduction in CNBP expression in tissue expressing APP(Swe). We conclude that expression of APP(Swe) in murine tissue induces a decrease in CNBP expression. This effect does not appear to be due to alterations in CNBP transcription. APP(Swe) expression may provide a tool for the study of CNBP regulation and clues to the roles of both proteins in disease.
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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.