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 β-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 APPSwe. We conclude that expression of APPSwe in murine tissue induces a decrease in CNBP expression. This effect does not appear to be due to alterations in CNBP transcription. APPSwe expression may provide a tool for the study of CNBP regulation and clues to the roles of both proteins in disease.
Original language | English |
---|---|
Pages (from-to) | 57-61 |
Number of pages | 5 |
Journal | Neuroscience Letters |
Volume | 482 |
Issue number | 1 |
DOIs | |
State | Published - Sep 2010 |
Bibliographical note
Funding Information:Supported by NIH grants NS058382, AG005119, and RR020171 . We would like to thank Dr. Frank LaFerla for the T7A6 mice, and Dr. Salvatore Oddo for the 3xTG mouse tissue. We would like to thank Dr. Christa M. Studzinski for the inception and preliminary data for the diet studies, and Marjorie Rochette for assistance in characterizing the CNBP antiserum.
Keywords
- APP
- Alzheimer's disease
- CNBP
- Sporadic inclusion body myositis
ASJC Scopus subject areas
- General Neuroscience