Comparison of methods for polycythemia rubra vera-1 mRNA quantification in whole-blood leukocytes and purified granulocytes.

Human mu opioid receptor gene polymorphisms and vulnerability to substance abuse. Sequence variations in the mu-opioid receptor gene (OPRM1) associated with human addiction to heroin. Sequence variability and candidate gene analysis in complex disease: association of mu opioid receptor gene variation with substance dependence. Mu opioid receptor gene variants: lack of association with alcohol dependence. Mol Psychiatry 1997;2:490 – 4. 17. Beyer AKT, Höllt V. A118G polymorphism does not alter the ligand binding and activity of the human mu-opioid receptor. polymorphism A118G of the human mu-opioid receptor gene decreases the clinical activity of morphine-6-glucuronide but not that of morphine. variability and candidate gene analysis in two cancer patients with complex clinical outcomes during morphine therapy. Does the A118G polymorphism at the mu-opioid receptor gene protect against morphine-6-glucuronide toxicity? Anesthesiology 2002;97:814 –9. variation S268P of the human mu-opioid receptor affects both desensitiza-tion and G protein coupling. A single-nucleotide polymorphic mutation in the human mu-opioid receptor severely impairs receptor signaling. Site mutation in the rat mu-opioid receptor demonstrates the involvement of calcium/calmodulin-dependent protein kinase II in agonist-mediated desensitization. Genetics of two mu opioid receptor gene (OPRM1) exon I polymorphisms: population studies, and allele frequencies in alcohol-and drug-dependent subjects. Single nucleotide polymorphisms in the human mu opioid receptor gene alter basal G protein coupling and calmodulin binding. In the absence of pathognomonic markers, the diagnosis of the two chronic myeloproliferative disorders polycy-themia vera (PV) and essential thrombocythemia (ET) has relied on a set of clinical and laboratory criteria (1–5). The cloning of the cell surface receptor polycythemia rubra vera-1 (PRV-1) has recently been described (6), and the consistent overexpression of PRV-1 mRNA observed in PV patients indicates that this might constitute a new diagnostic marker for the disease. In the initial cohort examined by Northern blot analysis, PRV-1 expression was increased in all PV patients examined as well as in some ET patients, but not in healthy controls (6). These results have also been verified and extended using a quantitative reverse transcription-PCR (RT-PCR) assay. All PV as well as 50% of ET patients displayed increased PRV-1 expression (7, 8). Patients with secondary erythro-cytosis and healthy controls tested showed PRV-1 concentrations within the reference interval. Interestingly, the observed increase in PRV-1 mRNA expression does not lead to a corresponding increase in protein expression on the cell surface (9). Erythropoietin-independent colony growth and PRV-1 overexpression seem to go hand in hand in both PV and …