Abstract
The members of the ADAR (adenosine deaminase acting on RNA) gene family are involved in site-selective RNA editing that changes adenosine residues of target substrate RNAs to inosine. Analysis of staged chimeric mouse embryos with a high contribution from embryonic stem cells with a functional null allele for ADAR1 revealed a heterozygous embryonic-lethal phenotype. Most ADAR1+/- chimeric embryos died before embryonic day 14 with defects in the hematopoietic system. Our results suggest the importance of regulated levels of ADAR1 expression, which is critical for embryonic erythropoiesis in the liver.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Deaminase / genetics*
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Adenosine Deaminase / metabolism
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Alleles
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Animals
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Chimera
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Embryonic and Fetal Development
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Erythroblasts / cytology
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Erythropoiesis*
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Female
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Hematopoietic Stem Cells / cytology*
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Hematopoietic Stem Cells / enzymology
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Hepatocytes / cytology
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Immunoenzyme Techniques
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Liver / cytology
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Liver / embryology*
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Liver / enzymology
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Mice
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Mice, Inbred BALB C
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Mice, SCID
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Phenotype
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RNA Editing*
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RNA-Binding Proteins
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Stem Cells / cytology
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Stem Cells / enzymology
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Teratoma / genetics
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Teratoma / pathology
Substances
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RNA-Binding Proteins
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ADARB1 protein, human
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Adenosine Deaminase