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

The CP-I subunit of calf kidney adenosine deaminase complexing protein (ADCP), isolated by affinity chromatography based on Sepharose-4B immobilized adenosine deaminase, is identical with dipeptidyl peptidase IV. This finding is based on the following results: (a) Its M(r) = 110 kD, as determined by sodium dodecyl sulphate polyacrylamide gel electrophoresis; (b) its catalytic activity toward Gly-Pro-p-nitroanilide; (c) its inhibition by serine protease inhibitor; and (d) by two peptide sequences resulting from its trypsin proteolysis. Accordingly, the CP-I subunit of ADCP isolated from bovine kidney is DPPIV (CD26). Thus, as anticipated, the high affinity between ADA subunits prevails even when they originate in different species.
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PMID:The CP-I subunit of adenosine deaminase complexing protein from calf kidney is identical to human, mouse, and rat dipeptidyl peptidase IV. 962 61

This study was carried out to determine the effects that human neutrophils have on permeability across a model of the blood-brain barrier (BBB) formed by primary cultures of bovine brain microvessel endothelial cells (BBMEC). Transendothelial electrical resistance (TEER) was used to measure changes in permeability across BBMEC monolayers in a dual compartment system, during neutrophil interactions. When neutrophils (5 x 10(6)/ml) were applied to monolayers, TEER increased (permeability decreased). Adenosine was implicated, since the TEER increase was blocked by adenosine deaminase (1 U/ml) and the adenosine A2 receptor antagonist ZM 241385 (at 10(-6) M but not 10(-8) M, implicating A2B receptors). Oxygen free radicals were implicated as the TEER increase was blocked by combined catalase (100 U/ml) and superoxide dismutase (60 U/ml). When a gradient of the bacterial chemoattractant peptide formyl methionyl leucine phenylalanine (fMLP, 10(-7) M) was applied to neutrophils, the TEER decreased (permeability increased), concurrent with migration. When fMLP (10(-7) M) was added to the neutrophils, without migration, no change occurred. The TEER decrease was blocked by loading endothelium with the calcium buffer BAPTA (10 microM) and partially blocked by the serine protease inhibitor aprotinin (20 microg/ml). Measures to block the potential extracellular triggers heparin binding protein, glutamate, oxygen free radicals and binding to intercellular cell adhesion molecule-1 (ICAM-1) were ineffective. These data indicate that neutrophils both reduce and increase permeability in a cell culture model of the BBB, correlated to their proximity and migration through the endothelium. They explore the role of neutrophils in BBB breakdown, and the formation or amelioration of vasogenic cerebral edema.
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PMID:Neutrophils both reduce and increase permeability in a cell culture model of the blood-brain barrier. 1475 93