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)

Four Bovidae cell lines (BEK-1, MDBK, Bu and EBTr) were characterized by means of enzymatic biochemical markers. Out of 15 enzymatic systems, 3--adenosine deaminase (Ada), phosphoglucomutase (Pgm) and nucleoside phosphorylase (Np)--were found to be polymorphic and quite suitable for biochemical identification of each cell line. The Bu cell line has shown a Np phenotypic pattern which could be distinctive of the Bison bison species.
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PMID:Isozyme characterization of cattle (Bos taurus) and American buffalo (Bison bison) cell cultures. 10 20

Methods for measuring enzymatic activity of adenosine deaminase from human erythrocytes were examined and compared with each other. Determination of ADA by the method in which adenosine is converted into inosine with uric acid as the final product by the action of nucleoside phosphorylase and xanthine oxidase appears to yield the most reliable results. In the recommended assay saponin is used for lysis of erythrocytes when testing adenosine deaminase activity in red blood cells. Storage of erythrocyte samples is optimal at +4 degrees C; storage at room temperature or at -20 degrees C leads to loss of adenosine deaminase activity.
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PMID:Quantitative measurement of adenosine deaminase from human erythrocytes. 24 May 21

Two familial enzymopathies, always related to the combined immune deficit, are reviewed. Both are clinically characterized by repeated infections since the birth, leading to fatal issue before age of 4 years. The hereditary deficiency of adenosine deaminase is associated to the deficient functions of T and B lymphocytes. The activity of the enzyme is non detectable in the erythrocytes, strongly reduced in the lymphocytes and in several organs. In hereditary deficiency of nucleoside phosphorylase the functional anomalies of T lymphocytes are observed. The biochemical mechanism of the relation between the two enzymopathies and the deficient function of the immune system is centered on the metabolic pathway of purine nucleosides ans nucleotides.
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PMID:[Familial immune deficit and genetic deficiency of adenosine deaminase or of nucleoside phosphorylase (author's transl)]. 30 93

Clear metabolic differences between T- and B-cells were demonstrated. Both adenosine deaminase (ADA) and nucleoside phosphorylase (NP) activities increased during logarithmic growth and then decreased in T-cells, but remained essentially constant during the growth cycle of B-cells. When these enzyme activities were examined in a number of T-cell, B-cell, and null cell lines, ADA activity was clearly higher in T-cells as compared to all others. With NP, the opposite appeared to be true, although the differences were much smaller and not statistically significant in all instances. No clear differences were found in the isoenzyme distributions of both enzymes in the various cell types.
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PMID:Differences in purine metabolizing enzyme activities in human leukemia T-cell, B-cell and null cell lines. 41 84

1. The haemoglobin content of developing erythroblasts was shown to increase rapidly when the cells completed the final cell division of erythroid development and passed from the dividing into the non-dividing cell compartment. 2. The activity of carbonic anhydrase was measured and shown to increase continually throughout erythroid differentiation. The activity increased most rapidly in the polychromatic stage. 3. Catalase activity did not increase significantly during erythroid differentiation until the reticulocyte stage. 4. The activity of four enzymes, glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, adenosine deaminase and nucleoside phosphorylase, exhibited a similar pattern of change during erythroid differentiation. In the dividing cell compartment their activity was relatively high but exhibited a steep decline between the polychromatic stage and the orthochromatic stage, that is, as the cell completed its final cell division and moved from the dividing to the non-dividing compartment. After this the activity of these enzymes was stabilized at a relatively low value, and this activity persisted at such a value until the reticulocyte stage. 5. Lactate dehydrogenase activity also declined after the cell had crossed from the dividing into the non-dividing stage, but in this case the decline was less than in the case of the above four enzymes. 6. Adenylate kinase activity was relatively constant in the dividing cell compartment but exhibited a 60 percent increase when the cell passed from the dividing into the non-dividing compartment. 7. The cessation of cell division appears to coincide with a set of complex biochemical changes.
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PMID:Biochemical and enzymic changes during erythrocyte differentiation. The significance of the final cell division. 80

Foals with combined immunodeficiency had normal levels of purine salvage pathway enzymes, including adenosine deaminase, nucleoside phosphorylase, and xanthine oxidase.
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PMID:Evaluation of adenosine deaminase and other purine salvage pathway enzymes in horses with combined immunodeficiency. 81 21

Blood samples from 509 Macushi and 623 Wapishana Amerindians of of Northern Brazil and Southern Guyana have been analyzed with reference to the occurrence of rare variants and genetic polymorphisms of the following 25 systems: (i) Erythrocyte enzymes: acid phosphatase-1, adenosine deaminase, adenylate kinase-k, carbonic anhydrase-1, carbonic anhydrase-2, esterase A1,2,3, esterase D, galactose-1-phosphate uridyltransferase, isocitrate dehydrogenase, lactate dehydrogenase, malate dehydrogenase, nucleoside phosphorylase, peptidase A, peptidase B, phosphoglucomutase 1, phosphoglucomutase 2, phosphogluconate dehydrogenase, phosphohexoseisomerase, triosephosphate isomerase and (ii) Serum proteins: albumin, ceruloplasmin, haptoglobin, hemoglobin A2 and transferrin. Fifteen different rare variants were detected, involving 11 of these systems. In addition, a previously undescribed variant of ESA 1,2,3 which achieves polymorphic proportions in both these tribes is described. Excluding this variant, the frequency of rare variants is 1.1/1000 in 12510 determinations in the Macushi and 4.7/1000 in 15396 determinations in the Wapishana. The ESA 1,2,3 polymorphism was not observed in 382 Makiritare, 232 Yanomama, 146 Piaroa, 404 Cayapo, 190 Kraho and 112 Moro. Irregularities in the intratribal distribution of this polymorphism in the Macushi and Wapishana render a decision as to the tribe of origin impossible at present. Gene frequencies are also given for previously described polymorphisms of 5 systems: haptoglobin, phosphoglucomutase 1, erythrocyte acid phosphatase, esterase D, and galactose-1-phosphate-uridyl-transferase.
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PMID:Genetic studies of the Macushi and Wapishana Indians. I. Rare genetic variants and a "private polymorphism' of esterase A. 87 Apr 12

Severe Combined Immunodeficiency (SCID) is a fatal disorder of infancy in which patients exhibit profound defects of both cellular and humoral immune function. Approximately 50% of patients with the autosomal recessive form of SCID have a genetically determined deficiency of the purine salvage enzyme adenosine deaminase (ADA). Prenatal diagnosis of SCID-ADA deficiency has been successful and detection of heterozygous carriers has been shown to be feasible. A mutation at the structural locus for ADA has been found in several cases but clinical heterogeneity indicates that genetic heterogeneity at the molecular level is to be expected. In vitro model studies and clinical course suggest that the pathophysiology may involve primarily an inhibition of T-cell maturation with lesser effects on B-cell maturation as well as "self-destruction" of differentiated cells following antigen stimulation. The culprit may be adenosine itself or one of its metabolites such as ATP or cAMP, which are elevated in these patients. Bone marrow transplantation remains the recommended mode of therapy but red cell transfusion may offer an alternative when bone marrow transplantation is not feasible. The finding that deficiency of the next enzyme in the purine salvage pathway, nucleoside phosphorylase, is also associated with an immune deficiency disorder suggests that integrity of the purine salvage pathway may be crucial for normal differentiation and function of immunocompetent cells in man.
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PMID:Adenosine deaminase deficiency and immunodeficiencies. 87 49

An improved screening test for both adenosine deaminase and nucleoside phosphorylase is described.
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PMID:A new screening method for adenosine deaminase and nucleoside phosphorylase. 125 77

A pair of ribonuclease assays have been developed which offer improvements in specificity, simplicity, and/or sensitivity over current procedures. The assays measure the rate of adenosine release upon ribonuclease hydrolysis of 3'-adenosyl dinucleoside monophosphate substrates. Adenosine formation is spectrophotometrically determined by combining a coupled-enzyme system (adenosine deaminase or an adenosine deaminase/nucleoside phosphorylase/xanthine oxidase combination) to the ribonuclease cleavage. As demonstrated by a brief characterization of the ribonuclease activities in several mouse tissues, the methods demonstrate the advantage of being able to discriminate between ribonucleases of differing substrate specificities. An interesting guanosyl(3'-5')adenosine-specific ribonuclease in mouse brain has been identified using these assay methods.
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PMID:Spectrophotometric ribonuclease assays using dinucleoside monophosphate substrates. 152 17


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