期刊
DEVELOPMENTAL NEUROSCIENCE
卷 31, 期 3, 页码 223-237出版社
KARGER
DOI: 10.1159/000210185
关键词
Prenatal development; Neuron; Serotonin; Inosine; Adenosine; Mouse; ADAR
资金
- US Public Health Service [NS33323, MH078028]
- NICHD core grant [P30HD15052]
- Vanderbilt Kennedy Center
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P30HD015052] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [P50MH078028] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS033323] Funding Source: NIH RePORTER
The conversion of adenosine to inosine within RNA transcripts is regulated by a family of double-stranded RNA-specific adenosine deaminases referred to as adenosine deaminases that act on RNA (ADARs). Little is known regarding the developmental expression of ADAR family members or the mechanisms responsible for the specific patterns of editing observed for ADAR substrates. We have examined the spatiotemporal expression patterns for ADAR1 and ADAR2 in mouse forebrain. ADAR1 and ADAR2 are broadly distributed in most regions of the mouse forebrain by P0, including the cerebral cortex, hippocampus, and diencephalon. High expression levels were maintained into adulthood. Colocalization studies demonstrated ADAR1 and ADAR2 expression in neurons but not astrocytes. Editing for specific ADAR mRNA targets precedes high expression of ADAR proteins, suggesting that region-specific differences in editing patterns may not be mediated solely by ADAR expression levels. Copyright (C) 2009 S. Karger AG, Basel
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