Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.107 (DAT)
1,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Iron deficiency (ID) is the most common nutritional deficiency worldwide especially among young children, women in pregnancy and breastfeeding. This study was undertaken to assess the prevalence of ID in 1288 pupil ranging in age from 11 to 14 years. Haemoglobin (Hb), mean corpuscular volume (MCV), mean corpuscular Hb (MCH), serum iron (Fe) serum transferrin (Trf), serum ferritin (Ft) and an inflammtory proteic profil (IPP) were measured. The IPP combines the analysis of protein variations: protein results are converted in percent of normal values referenced for the technique used. It has been suggested that on the protein profile, an increase in serum transferrin level compared to a normal serum albumin level (DAT: difference albumin-transferrin), appears early in the course of ID. Iron deficiency was defined by a low serum ferritin (< 15 ng/mL) and/or a pathologic DAT (> 28%). Approximately, 33.8% of children had Ft < 15 ng/mL and 12,8% had DAT > 28% while ferritin values were in the normal range. Diagnosis performance (sensitivity, specificity and diagnosis efficacy) of ferritin and DAT were compared to the performance of high serum transferrin receptor (sTfR) values in 2 populations presenting or not a biological inflammation. Only the diagnosis efficacy of DAT was constant in both situations. In conclusion, the serum ferritin concentration is the first indicator of body storage iron identifying ID, however normal or elevated values of ferritin may be difficult to interpret particulary in the presence of inflammation. sTfR and DAT values are thus reliable indicators of ID in such circumstances.
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PMID:[Difference albumin-transferrin interest in the iron deficiency detection in a cohort of 1288 schoolchildren in the district of Tunis]. 1716 59

Amphetamine (AMPH) is a potent dopamine (DA) transporter (DAT) inhibitor that markedly increases extracellular DA levels. In addition to its actions as a DAT antagonist, acute AMPH exposure induces DAT losses from the plasma membrane, implicating transporter-specific membrane trafficking in amphetamine's actions. Despite reports that AMPH modulates DAT surface expression, the trafficking mechanisms leading to this effect are currently not defined. We recently reported that DAT residues 587-596 play an integral role in constitutive and protein kinase C (PKC)-accelerated DAT internalization. In the current study, we tested whether the structural determinants required for PKC-stimulated DAT internalization are necessary for AMPH-induced DAT sequestration. Acute amphetamine exposure increased DAT endocytic rates, but DAT carboxy terminal residues 587-590, which are required for PKC-stimulated internalization, were not required for AMPH-accelerated DAT endocytosis. AMPH decreased DAT endocytic recycling, but did not modulate transferrin receptor recycling, suggesting that AMPH does not globally diminish endocytic recycling. Finally, treatment with a PKC inhibitor demonstrated that AMPH-induced DAT losses from the plasma membrane were not dependent upon PKC activity. These results suggest that the mechanisms responsible for AMPH-mediated DAT internalization are independent from those governing PKC-sensitive DAT endocytosis.
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PMID:Amphetamine-induced decreases in dopamine transporter surface expression are protein kinase C-independent. 1816 41