Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transferrin receptor (TR) performs the major function of binding and internalizing its specific iron-loaded ligand, transferrin, and its expression is closely linked to the proliferation status of the cell. This study was undertaken to elucidate TR expression in the hyperplastic lesion of hepatocyte in chemically induced hepatic carcinogenesis. The resistant hepatocyte model was chosen for a rat model of carcinogenesis and Sprague-Dawley rats were divided into the following groups: the control groups of normal diet and iron-rich diet with or without hydroxyquinoline and the groups of carcinogen alone and carcinogen plus iron-rich diet with or without administration of hydroxyquinoline. Microscopic changes in the liver, expression of transferrin receptor and glucose-6-phosphatase were studied. The hepatocyte of the control group showed both cytoplasmic and membranous expression of TR. The liver of rats fed on high iron diet accumulated iron and the expression of TR was down regulated by intrahepatic iron accumulation. In the carcinogen administered group the resistant hepatocyte of hyperplastic lesion revealed strong membranous expression of TR and failed to accumulate iron in spite of high iron diet but in contrast the surrounding non-resistant hepatocyte expressed TR in both the membrane and cytoplasm and stored iron when fed on high iron diet. The strong membranous expression of TR is one of the characteristics of the resistant hepatocyte of hyperplastic lesion and it seems to be related to the inability to accumulate iron in spite of a high iron diet.
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PMID:Transferrin receptor expression of the hyperplastic lesions of hepatocyte in experimental hepatocarcinogenesis. 852 44

For the application of microarray technology as an additional endpoint in toxicological studies, there is a need to understand associations between pathological processes and gene expression alterations. In the current study, we investigated gentamicin as a nephrotoxic model compound. Gene expression changes of the kidney in response to a dose of 80 mg/kg gentamicin were analyzed by using DNA microarray technology and alterations in gene expression were associated with results from conventional histopathological investigations and with the described pathomechanisms of gentamicin. Under the conditions of our experiment, the mRNA level of 211 genes were found to be deregulated by gentamicin. The gentamicin-induced affection of proximal convoluted tubules was associated with a strong up-regulation of mRNAs encoding for proteins which are used as nephrotoxicity markers in urine and plasma such as Kim-1, Osteopontin and TIMP1. Candidate marker genes for nephrotoxicity such as GATM were deregulated. Gentamicin-induced lysosomal phospholipidosis was indicated by deregulation of lysosomal located gene products such as ATP6V1D, a subunit of the lysosomal H+ transporting ATPase. Effects on glucose transport and metabolism were indicated by the down-regulation on SGLT-2 and glucose-6-phosphatase. Renal cell apoptosis was indicated by up-regulated genes as TP53 and BAX. The role of oxidative stress in gentamicin toxicity was reflected by deregulation of transferrin receptor and heme oxygenase. The results of the study show the potential of microarray technology to study a complex mechanism of toxicity in a single study.
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PMID:Identification of genes involved in gentamicin-induced nephrotoxicity in rats--a toxicogenomic investigation. 1966 12