Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.7 (DNA polymerase)
 17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the prevalence of the sickle cell gene (betaS) in Yemen and amongst people from different regions of the country living in the capital, Sana'a City, cord blood samples from 1,500 consenting mothers were collected from hospitals in Sana'a City between July and December 2001. The names and original homes of the parents were recorded. Cation exchange high performance liquid chromatography (HPLC) analysis was used for screening, while isoelectric focusing (IEF) and DNA polymerase chain reaction (PCR) were used to confirm Hb S [beta6(A3)Glu-->Val]. Thirty-three samples were found to show Hb FAS, giving an overall likely betaS gene frequency of 0.011. The betaS gene frequency varied with the part of the country from which the parents came. Amongst people from Taiz and Haja in the west, the gene frequency was more than 0.04, but less than 0.004 amongst people from Ibb, adjacent to the governorate (administrative division) of Taiz. Of 66 chromosomes from babies carrying the betaS gene, only 1.5% also carried the -158 (C-->T) Ggamma-globin gene XmnI site compared with 16.1% of 168 chromosomes from babies without the betaS gene from the same regions. The results of this study show a higher betaS gene frequency in the western coastal part of Yemen than in the central mountainous and eastern desert areas. The incidence of affected homozygous births may therefore reach 20/10,000 in certain areas, although it is much lower than this overall. Limited health resources can best be invested in developing a program of education, screening and health care, initially prioritizing those communities residing in the western areas of Yemen with the highest betaS gene frequency.
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PMID:Prevalence of the sickle cell gene in Yemen: a pilot study. 1565 86

The main target organ of the mycotoxin ochratoxin A (OTA) in mammals is the kidney but OTA has also been shown to be hepatotoxic in rats and to induce tumors in mouse liver. Even at very low concentrations, OTA causes perturbations of cellular signaling pathways as well as enhanced apoptosis. OTA has been extensively studied in kidney cell systems. Since this substance also affects liver health, we focused our work on apoptosis-related events induced by OTA in primary rat hepatocytes. We performed pathway-specific polymerase chain reaction arrays to assess the expression of genes involved in apoptosis. Treatment with 1 microM OTA for 24 h caused marked changes in apoptosis-related gene expression. Genes as apaf1, bad, caspase 7, polb (DNA polymerase beta, performs base excision repair), and p53, which are marker genes for DNA damage, were upregulated. FAS and faslg were also markedly induced by treatment with OTA. Treatment of hepatocytes with OTA led to a concentration-dependent inhibition of protein biosynthesis. Apoptosis-inducing factor was released from mitochondria following OTA treatment; the mycotoxin induced the activity of caspases 8, 9, and 3/7 and caused chromatin condensation and fragmentation. Caspase inhibition led to a significant but not complete reduction of OTA-induced apoptosis. Our data suggest that not only OTA leads to p53-dependent apoptosis in rat hepatocytes but it also hints to other mechanisms, independent of caspase activation or protein biosynthesis, being involved.
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PMID:Characterization of ochratoxin A-induced apoptosis in primary rat hepatocytes. 1956 91