Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

2',5'-oligoadenylate synthetase (2-5OAS) has been studied in peripheral blood mononuclear cells from nine patients with hairy cell leukaemia (HCL) receiving therapy with the adenosine deaminase inhibitor deoxycoformycin (dCF) or alpha interferon (alpha-IFN). 2-5OAS mRNA was assayed by dot-blot hybridization. Increase of 2-5OAS mRNA level was seen in six patients with HCL treated with dCF and in one patient treated with alpha-IFN who responded to therapy. A patient with a variant form of HCL treated with dCF and the second patient treated with alpha-IFN did not show an increase of 2-5OAS mRNA and neither responded to therapy. The 15 other patients with T or B-chronic lymphoblastic leukaemia (CLL), T-acute lymphoblastic leukaemia (ALL), adult T-cell leukaemia lymphoma (ATLL), non-Hodgkins lymphoma (NHL), Sezary and T or B-prolymphocytic leukaemia (PLL) treated with dCF did not show an increase in 2-5OAS, though four patients, all with T-cell tumours, responded clinically. 2-5OAS activity is known to be stimulated by alpha-IFN and recent work suggests that this rise in 2-5OAS may result in increased cleavage of mRNA for tumour necrosis factor (TNF) and other cytokines on which autocrine growth and proliferation of the tumour cells are dependent. By analogy, we suggest that one mechanism of action of dCF in hairy cell leukaemia may be to break down an autocrine growth loop for TNF or other cytokines. An alternative explanation for these observations is that cytokines released from hairy cells in the bone marrow killed by dCF induce a rise in 2-5OAS in circulating leucocytes.
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PMID:Increase in 2',5'-oligoadenylate synthetase caused by deoxycoformycin in hairy cell leukaemia. 155 Jul 76

The concentration of gamma interferon (IFN gamma) and adenosine deaminase (ADA) activity were measured in the pleural fluid of 162 patients to compare their diagnostic significance and to establish a possible correlation between both tests. The IFN gamma levels in tuberculous pleural effusions were quite variable, with a mean of 93 U/ml and a median of 48 U/ml. They were higher than 2 U/ml in all cases, whereas no case of nontuberculous effusion showed higher values. ADA activity was higher than 43 U/l in all tuberculous effusions, with a mean value of 80 U/l, higher than in any other group except lymphoma. In three pleural effusions associated with lymphoma, one with mesothelioma, one with adenocarcinoma and four with empyema, ADA activity was higher than 43 U/l. In these patients, IFN gamma levels were low. There was no correlation in the whole series or in any group between IFN and ADA. Both parameters can be very useful for the diagnosis of tuberculous pleuritis. The measurement of IFN gamma is more specific, although the experience with this test is more limited than with ADA. It has the additional shortcoming of a high cost and it requires facilities for radionuclide use. Therefore, we think that ADA measurement should be considered as a routine test while IFN gamma measurement should be reserved for reference institutions.
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PMID:[Gamma interferon and adenosine deaminase in pleuritis]. 211 Jun 5

It has been found that both adenosine deaminase (ADA) and gamma-interferon (r-IFN) are higher in tuberculous pleural effusions than in other types of pleural effusion. Both mechanisms may be related to the T-lymphocytes in effusions. We studied 39 pleural effusions: 19 tuberculous and 20 malignant [The ADA was determined according to the Giusti method and r-IFN by ELISA]. We compared the ADA and r-IFN levels in both groups of effusions and tried to determine if there was any correlation between them. The results showed: (1) The ADA enzyme level was significantly higher in tuberculous effusions than in malignant effusions as was expected (133.0 +/- 50.4 vs 32.0 +/- 17.7 U/L). (2) The r-IFN was also significantly higher in tuberculous effusions than in malignant effusions (30.4 +/- 17.4 vs 2.9 +/- 2.8 U/ml). (3) The coefficients of regression for the ADA and r-IFN levels were poor. In conclusion, both tests for measuring ADA and r-IFN levels are excellent methods for differentiating tuberculous and malignant effusions, and especially measurement of the r-IFN level could serve as a more specific test for differentiating malignant pleural effusions with high ADA levels. However, no strong correlation was found between the ADA and r-IFN levels.
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PMID:Diagnostic value of adenosine deaminase and gamma-interferon in tuberculous and malignant pleural effusions. 251 12

Treatment of human amnion U cells with interferon increased the steady state level of mRNA encoding the double-stranded (ds) RNA-specific adenosine deaminase (AdD) as measured by Northern gel-blot analysis. A single major dsRNA-specific AdD transcript of approximately 6.7 kb was detected; the transcript was induced by both interferon-alpha (IFN-alpha) and interferon-gamma (IFN-gamma). Likewise, Western immunoblot analysis revealed that a 150-kDa protein recognized by antiserum prepared against recombinant dsRNA-specific AdD was increased in the human amnion U and neuroblastoma SH-SY5Y cell lines treated with interferon. Both IFN-alpha and IFN-gamma induced the 150-kDa protein. These results, which establish that dsRNA-specific AdD is an IFN-inducible protein in human cells, have implications regarding the possible role of interferon in persistent viral infections.
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PMID:Mechanism of interferon action: double-stranded RNA-specific adenosine deaminase from human cells is inducible by alpha and gamma interferons. 761 88

The gamma interferon (gamma-IFN) concentration and the adenosine deaminase (ADA) activity were evaluated in 30 patients with tuberculous peritonitis, 21 patients with ascites due to a malignant disorder, and 41 patients with cirrhosis. The gamma-IFN concentrations were significantly higher (p < 0.0001) in tuberculous peritonitis patients (mean: 6.70 U/ml) than in the malignant (mean: 3.10 U/ml) and cirrhotic (mean: 3.08 U/ml) groups. Use of a cut off value of > or = 3.2 U/ml gave the assay a sensitivity of 93% (25 of 27), a specificity of 98% (54 of 55), positive (P+) and negative (P-) predictive values of 96% and a test accuracy of 96%. The ADA activity was significantly (p < 0.0001) higher in the tuberculous peritonitis group (mean: 101.84 U/l) than in the control groups (cirrhosis (mean: 13.49 U/l) and malignancy (mean: 19.35 U/l)). A cut off value of > 30 U/l gave the ADA test a sensitivity of 93% (26 of 28) a specificity of 96% (51 of 53), a (P+) value of 93%, a (P-) value of 96%, and a test accuracy of 95%. There was a significant (p < 0.0001) correlation (r = 0.72) between ADA activity and gamma-IFN values in patients with tuberculous peritonitis. These results show that a high concentration of gamma-IFN in ascitic fluid is as valuable as the ADA activity in the diagnosis of tuberculous peritonitis. Both are rapid non-invasive diagnostic tests for tuberculous peritonitis.
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PMID:Ascitic fluid gamma interferon concentrations and adenosine deaminase activity in tuberculous peritonitis. 769 2

The diagnosis of tuberculous ascites is often difficult because of the subtle clinical clues, poorly discriminative biochemical assays, delayed results of bacteriological studies and hazards of laparoscopy. Therefore, the role of ascites adenosine deaminase (ADA) activity and interferon-gamma (IFN-delta) level in distinguishing tuberculous from other causes of ascites was examined in 50 patients with ascites. Following bacteriologic culture, seventeen (34%) patients were found to have tuberculous ascites; nine (59.9%) of them had also schistosomal hepatic fibrosis (SHF). Therefore, 36% (9 out of 25) of all patients with SHF included in the study, had coexistent peritoneal tuberculosis despite the presence of transudative ascites and unrecognized clinical features. Ascites ADA activity was significantly higher in tuberculous than in other causes of ascites (P < 0.001) regardless of the presence of an underlying liver disease. A cut-off of 28 U/L reached a sensitivity of 94.4% and a specificity of 100%. A direct correlation was found between ascites ADA activity and total proteins in the tuberculous group (r = 0.613) and the only false-negative result occurred in a patient with SHF and low-ascites protein. Ascites IFN-delta level was also significantly higher in tuberculous ascites with or without SHF than in other causes of ascites (P < 0.05). A cut-off of 26 pg/ml reached a sensitivity of 81% and a specificity of 100%. There was no correlation between ascites ADA activity and IFN-delta level in the tuberculous group (r = 0.329). Based on the results of the present study, it can be concluded that tuberculous ascites should be considered as an important cause of ascites particularly in patients with underlying liver disease. Ascites ADA activity was more sensitive than ascites IFN-delta in diagnosing tuberculosis (TB). It has proved to be an easy, rapid, safe and reliable method for routine use in the early diagnosis of tuberculous ascites.
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PMID:The value of ascites adenosine deaminase activity and interferon gamma level in discriminating tuberculous from non-tuberculous ascites. 816 54

We compared the parameters pleural adenosine deaminase (PADA, determined in 405 patients), the PADA/serum ADA ratio (P/SADA; 276 cases), pleural lysozyme (PLYS, 276 cases), the PLYS/serum LYS ratio (P/SLYS; 276 cases), and pleural interferon gamma (IFN, 145 cases) regarding their ability to differentiate tuberculous pleural effusions from others. The 405 pleural effusions were classified by previously established criteria as tuberculous (91), neoplastic (110), parapneumonic (58), empyemas (10), transudates (88), or miscellaneous (48). The intermean differences between the tuberculous group and each of the others were statistically significant for all five parameters (p < 0.01 for PLYS and P/SLYS with respect to the empyema group; p < 0.001 otherwise), except for PADA and P/SADA with respect to the empyema group. All the tuberculous pleurisy cases had PADA values of 47 U/L or more, as compared to only 5 percent of the other cases (sensitivity, 100 percent; specificity, 95 percent). P/SADA was above 1.5 in 85.7 percent of tuberculous effusions and 11 percent of the others (sensitivity, 85.7 percent; specificity, 89 percent). PLYS, with a diagnostic threshold of 15 g/ml, had a sensitivity of 85.7 percent and a specificity of 61.6 percent; P/SLYS, with a threshold of 1.1, had a sensitivity of 67.3 percent and a specificity of 90.3 percent; and IFN, with a threshold of 140 pg/ml, had a sensitivity of 94.2 percent and a specificity of 91.8 percent. The lowest misclassification rate was achieved by PADA, with statistically significant differences (p < 0.001) with respect to P/SADA, PLYS, and P/SLYS, but not with respect to IFN. The only significant pairwise correlations among these parameters were between P/SLYS and PADA and between P/SLYS and P/SADA. We conclude that PADA and IFN are useful parameters for early diagnosis of tuberculous pleurisy, and that the other parameters considered have no advantages over PADA and IFN for this purpose (though the high specificity of P/SLYS may be noted).
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PMID:Diagnosis of tuberculous pleurisy using the biologic parameters adenosine deaminase, lysozyme, and interferon gamma. 820 19

Reovirus induces IFN, and reovirus is sensitive to the antiviral actions of IFN. The characteristics of the IFN-inducing capacity of reovirus, and the antiviral actions of IFN exerted against reovirus, are dependent upon the specific combination of reovirus strain, host cell line, and IFN type. Responses, both IFN induction and IFN action, differ quantitatively if not qualitatively and are dependent upon the virus, cell, and IFN combination. Stable natural dsRNA, identified as the form of nucleic acid that constitutes the reovirus genome, is centrally involved in the function of at least three IFN-induced enzymes. Protein phosphorylation by PKR, RNA editing by the ADAR adenosine deaminase, and RNA degradation by the 2',5'-oligoA pathway all involve dsRNA either as an effector or as a substrate. Considerable evidence implicates PKR as a particularly important contributor to the IFN-induced antiviral state displayed at the level of the single virus-infected cell, where the translation of viral mRNA is often observed to be inhibited following treatment with IFN-alpha/beta. In the whole animal infected with reovirus, elevated cellular immune responses mediated by enhanced expression of MHC class I and class II antigens induced by IFN-alpha/beta or IFN-gamma may contribute significantly to the overall antiviral response.
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PMID:Reoviruses and the interferon system. 959 35

Interferon-alpha 2b (IFN-alpha 2b) can exert antiproliferative activity in both normal and malignant liver tissue. To study mechanisms of its antiproliferative action, the activity of the enzymes of adenosine metabolism were investigated. We studied 5'-nucleotidase (an adenosine-producing enzyme) and adenosine deaminase (involved in adenosine degradation). Female Wistar rats (3 weeks old) were treated with IFN-alpha 2b for 48 h, as were adult rats (3 months old) and adult rats subjected to partial hepatectomy. During IFN-alpha 2b administration, the activity of 5'-nucleotidase increased in the liver of 3-week-old rats, proportionately more than in adult rats, but the greatest increase was seen in partially hepatectomised rats. The activity of adenosine deaminase decreased in the liver of 3-week-old rats, did not change significantly in 3-month-old rats, but was significantly lower in partially hepatectomised rats. As high adenosine concentrations are toxic for mammalian cells, especially during proliferation, the progressive increase of adenosine production, together with the progressive decrease of its degradation, could be one of the mechanisms of IFN-alpha 2b-induced antiproliferative activity. In vitro studies were performed using collagenase-isolated hepatocytes. They were exposed to IFN-alpha 2b, a cAMP analogue, or both. The incubation of hepatocytes with IFN-alpha 2b did not significantly change the activity of both enzymes, whereas incubation with the cAMP analogue decreased 5'-nucleotidase activity and increased adenosine deaminase activity. The mechanism of IFN-alpha 2b-induced alteration in adenosine metabolism is therefore unclear.
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PMID:Different responses of rat liver adenosine metabolizing enzymes during in vivo and in vitro treatment with interferon-alpha 2b. 979 20

RNA-specific adenosine deaminase (ADAR1) catalyzes the deamination of adenosine to inosine in viral and cellular RNAs. Two size forms of the ADAR1 editing enzyme are known, an IFN-inducible approximately 150-kDa protein and a constitutively expressed N-terminally truncated approximately 110-kDa protein. We have now identified alternative exon 1 structures of human ADAR1 transcripts that initiate from unique promoters, one constitutively expressed and the other IFN inducible. Cloning and sequence analyses of 5'-rapid amplification of cDNA ends (RACE) cDNAs from human placenta established a linkage between exon 2 of ADAR1 and two alternative exon 1 structures, designated herein as exon 1A and exon 1B. Analysis of RNA isolated from untreated and IFN-treated human amnion cells demonstrated that exon 1B-exon 2 transcripts were synthesized in the absence of IFN and were not significantly altered in amount by IFN treatment. By contrast, exon 1A-exon 2 transcripts were IFN inducible. Transient transfection analysis with reporter constructs led to the identification of two functional promoters, designated PC and PI. Exon 1B transcripts were initiated from the PC promoter whose activity in transient transfection reporter assays was not increased by IFN treatment. The 107-nt exon 1B mapped 14.5 kb upstream of exon 2. The 201-nt exon 1A that mapped 5.4 kb upstream of exon 2 was initiated from the interferon-inducible PI promoter. These results suggest that two promoters, one IFN inducible and the other not, initiate transcription of the ADAR1 gene, and that alternative splicing of unique exon 1 structures to a common exon 2 junction generates RNA transcripts with the deduced coding capacity for either the constitutively expressed approximately 110-kDa ADAR1 protein (exon 1B) or the interferon-induced approximately 150-kDa ADAR1 protein (exon 1A).
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PMID:Human RNA-specific adenosine deaminase ADAR1 transcripts possess alternative exon 1 structures that initiate from different promoters, one constitutively active and the other interferon inducible. 1020 Mar 12


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