Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.17 (adenosine deaminase)
 5,206 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pregnant rats of 19th and 21st days were given an acute nitrogen overload produced by an infusion of either 0.2 M ammonium acetate or 0.2 M glutamine. Metabolic adaptations to nitrogen excess were studied measuring--in fetomaternal unit--non-protein nitrogen content and the activities of enzymes related with ammonia metabolism. Maternal and fetal plasma urea levels were increased by ammonium acetate treatment. Glutamine overload increased more the amino acid content in the mothers than in conceptus. As response to ammonium acetate treatment, glutamate dehydrogenase activity in liver was more sensitive in pregnant than in nonpregnant rats, suggesting more nitrogen incorporation into amino acids in pregnancy. Regarding glutamine synthetase activity, both treatments had an opposite effect except in kidney. The adenylate deaminase activity of pregnant rats was inhibited similarly to nonpregnant rats by nitrogen overloads, but stronger after glutamine infusion. Placenta and fetal metabolism were adjusted, as the dams, to lack of ammonia production by nitrogen overloads and to glutamine synthesis by ammonium acetate infusion.
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PMID:Metabolic adaptations to nitrogen excess in late gestation in rat. 177 94

Nucleotides, nucleosides and purine bases in trichloroacetic acid extracts of freeze clamped samples of human placenta have been measured by high-pressure liquid chromatography. The concentrations of the nucleotides concerned with energy transduction, ATP, ADP and AMP, and especially the energy charge, are stable over periods of ischaemia of 30 min. Concentrations of 14 nucleotides, including UDPAG, GDP Man, UDP and CTP, have now been defined. In addition, the concentrations of hypoxanthine, xanthine, uridine, adenine and inosine are indicated. Concentrations of the vasodilator adenosine are similar to the apparent Michaelis constants of its main metabolizing enzymes adenosine kinase and adenosine deaminase. The availability of 'normal' values of adenine nucleotide concentrations in human placenta should permit the detection of 'placental insufficiency' of energy supply, if this condition exists.
Placenta
PMID:Nucleotide, nucleoside and purine base concentrations in human placentae. 707 37

The formation of the trophoblast cell lineage of the placenta is one of the first developmental events to occur in mammalian embryogenesis. To understand the mechanisms of gene regulation in the trophoblast cell lineage we have used the murine adenosine deaminase gene (Ada) as a model. Ada is highly expressed in trophoblast cells of the placenta and is critical for embryo development. A 770bp fragment of the mouse Ada 5' flanking region is capable of directing trophoblast cell-specific expression in a transgenic model system. Earlier studies identified several critical portions of this fragment, including three footprinting regions that are necessary for correct gene expression in the placenta. Using electromobility shift assays (EMSA), we identified a 5bp sequence within footprint 3 that computer databases predicted bound to the transcription factor RUNX1 (also known as acute myeloid leukemia 1). This prediction was confirmed by supershift analysis using antibodies specific for RUNX1. The functional importance of this binding was demonstrated by both transient transfections and transgenic approaches. A significant reduction in expression of the reporter gene in the placenta was seen when the 5bp RUNX1 binding site was mutated. The findings reported here indicate that the RUNX1 transcription factor plays a significant role in regulating Ada gene expression in the trophoblast cell lineage.
Placenta
PMID:Regulation of murine Ada gene expression in the placenta by transcription factor RUNX1. 1633 72