Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-nine patients with homozygous sickle cell anaemia, 17 heterozygous individuals and 22 controls were investigated in respect to serum (S) 5'nucleotidase (5'NT, EC 3.1.3.5). The patients showed a significantly higher mean value of S-5'NT compared to the controls. However, this rise was heterogeneous as it occurred only among a subgroup of patients. The heterozygous individuals were not different from either the patients or the controls generating a situation which puts the heterozygous individuals in an intermediate position between the patients and the controls. S-5'NT showed significant correlation with S-bilirubin, S-aspartate aminotransferase, S-alanine aminotransferase and especially S-gammaglutamyl transferase. However, it was not correlated with S-alkaline phosphatase, which is another marker for hepatobiliary disease. These results suggest that the liver involvement in a subgroup of patients with sickle cell anaemia is a mixture of hepatocyte damage and the biliary tree involvement.
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PMID:Increased activity of 5' nucleotidase in serum of patients with sickle cell anaemia. 790 22

The precise molecular mechanisms underlying priapism associated with sickle cell disease remain to be defined. However, there is increasing evidence that upregulated activity of the opiorphin and adenosine pathways in corporal tissue, resulting in heighted relaxation of smooth muscle, have an important role in development of priapism. A key enzyme in the adenosine pathway is CD73, an ecto-5'-nucleotidase (5'-ribonucleotide phosphohydrolase; EC 3.1.3.5) which catalyzes the conversion of adenosine mononucleotides to adenosine. In the present study we investigated how sickle cell disease and hypoxia regulate the interplay between opiorphin and CD73. In the corpora of sickle cell mice we observed significantly elevated expression of both the mouse opiorphin homolog mSmr3a (14-fold) and CD73 (2.2-fold) relative to non-sickle cell controls at a life stage before the exhibition of priapism. Sickle cell disease has a pronounced hypoxic component, therefore we determined if CD73 was also modulated in in vitro corporal smooth muscle (CSM) models of hypoxia. Hypoxia significantly increased CD73 protein and mRNA expression by 1.5-fold and 2-fold, respectively. We previously demonstrated that expression of another component of the adenosine signaling pathway, the adensosine 2B receptor, can be regulated by sialorphin (the rat opiorphin homolologue), and we demonstrate that sialorphin also regulates CD73 expression in a dose- and time-dependent fashion. Using siRNA to knockdown sialorphin mRNA expression in CSM cells in vitro, we demonstrate that the hypoxic upregulation of CD73 is dependent on the upregulation of sialorphin. Overall, our data provide further evidence to support a role for opiorphin in CSM in regulating the cellular response to hypoxia or sickle cell disease by activating smooth muscle relaxant pathways.
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PMID:Opiorphin-dependent upregulation of CD73 (a key enzyme in the adenosine signaling pathway) in corporal smooth muscle cells exposed to hypoxic conditions and in corporal tissue in pre-priapic sickle cell mice. 2583 66