Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of the enzyme adenosine deaminase (ADA) decreases in the course of the differentiation of the human promyelocytic leukemic cell line HL-60, dependent on the pathway chosen. Differentiation to monocytes as induced by the phorbol ester TPA leads to a 50% reduction of enzyme activity. Induction to myeloid cells as induced by DMSO has a slower and less extensive (75% remaining activity) effect. The reduction in ADA enzymatic activity is preceded by a 5-10 fold reduction in ADA-specific mRNA which is also more rapid during TPA-induced differentiation. In contrast, c-myc mRNA expression is both in TPA- and DMSO-induced differentiation reduced to less then 5% of its initial level within 4h. Nuclear run-on analysis revealed that the reduction of c-myc-mRNA expression during both TPA- and DMSO-induced differentiation could be ascribed to the abolition of transcription of the third exon, whereas no change in the transcription of the first exon could be observed. No change could be detected in the rate of transcription of either the 5' and 3' parts of the ADA gene during TPA- and DMSO-induced differentiation, indicating that the expression of the ADA gene in HL-60 is controlled at a posttranscriptional level.
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PMID:Adenosine deaminase mRNA expression is regulated posttranscriptionally during differentiation of HL-60 cells. 330 3

High concentrations of adenosine (Ado), when added to L1210 lymphocytic leukemia cells, resulted in apoptosis or programmed cell death. The apoptotic process was accompanied by distinct morphological changes including chromatin condensation and blebbing of plasma membranes. Extensive DNA fragmentation was correlated with Ado concentrations. Furthermore, apoptosis in these cells was preceded by an early but transient expression of c-myc proto-oncogene, and was not influenced by homocysteine thiolactone added to the cells. Since severe combined immunodeficiency (SCID) is associated with a deficiency of adenosine deaminase, leading to defects in both cellular and humoral immunity, Ado-induced apoptosis may thus be a contributing factor in the pathology of SCID. Copyright 1994 S. Karger AG, Basel
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PMID:Induction of Apoptosis and c-myc in L1210 Lymphocytic Leukemia Cells by Adenosine. 1172 19

DNA replication initiates at origins within the genome. The late-firing murine adenosine deaminase (mAdA) origin is located within a 2 kb fragment of DNA, making it difficult to examine by realtime technology. In this study, fine mapping of the mAdA region by measuring the abundance of nascent strand DNA identified two origins, mAdA-1 and mAdA-C, located 397 bp apart from each other. Both origins conferred autonomous replication to plasmids transfected in murine embryonic fibroblasts (MEFs), and exhibited similar activities in vivo and in vitro. Furthermore, both were able to recruit the DNA replication initiator proteins Cdc6 and Ku in vitro, similar to other bona fide replication origins. When tested in a murine Ku80(-/-) cell line, both origins exhibited replication activities comparable to those observed in wildtype cells, as did the hypoxanthine-guanine phosphoribosyltransferase (HPRT) and c-myc origins. This contrasts with previously published studies using Ku80-deficient human cells lines and suggests differences in the mechanism of initiation of DNA replication between the murine and human systems.
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PMID:Fine mapping and functional activity of the adenosine deaminase origin in murine embryonic fibroblasts. 1818 Nov 56