Disruption of the adenosine deaminase gene causes hepatocellular impairment and perinatal lethality in mice

Maki Wakamiya, Michael R. Blackburn, Roland Jurecic, Mark J. McArthur, Robert S. Geske, Joiner Cartwright, Kohnosuke Mitani, Sukeshi Vaishnav, John W. Belmont, Rodney E. Kellems, Milton J. Finegold, Charles A. Montgomery, Allan Bradley, C. Thomas Caskey

Research output: Contribution to journalArticle

117 Scopus citations

Abstract

We have generated mice with a null mutation at the Ada locus, which encodes the purine catabolic enzyme adenosine deaminase (ADA, EC 3.5.4.4). ADA-deficient fetuses exhibited hepatocellular impairment and died perinatally. Their lymphoid tissues were not largely affected. Accumulation of ADA substrates was detectable in ADA-deficient conceptuses as early as 12.5 days postcoitum, dramatically increasing during late in utero development, and is the likely cause of liver damage and fetal death. The results presented here demonstrate that ADA is important for the homeostatic maintenance of purines in mice.

Original languageEnglish (US)
Pages (from-to)3673-3677
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume92
Issue number9
DOIs
StatePublished - Apr 25 1995

ASJC Scopus subject areas

  • General

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