Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The reverse transcriptase-polymerase chain reaction (RT-PCR) and direct sequencing were employed in the diagnosis and typing of foot-and-mouth disease virus (FMDV) in samples taken during the 1994 disease outbreak in Israel. Using PCR, virus isolation and serological methods it was shown that the 1994 disease outbreak in Israel and other Middle-Eastern countries was caused by O1 type virus. Direct PCR sequencing of VP1 genes and homology analysis of the virus isolates revealed that there were two distinct outbreaks in Israel. The first originated in Jordan, moved to the West Bank territory and then to the Lower Galilee. The second outbreak, caused by another virus, was responsible for disease outbreaks in South Lebanon, Upper Galilee and the Golan Heights. When viral sequences of isolates from the 1993 outbreaks in Egypt and Lebanon were included in the analysis, they showed a high degree of VP1 sequence homology between themselves, suggesting a common origin.
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PMID:Molecular epidemiology of foot-and-mouth disease (FMD) in Israel in 1994 and in other Middle-Eastern countries in the years 1992-1994. 750 79

Complement proteins in serum are mainly synthesized by hepatocytes. Recently, many cell types have been reported to synthesize complement in various tissues. In this study, we report the synthesis and secretion of the third component of complement (C3) by cultured glomerular epithelial cells (GEC). Using reverse transcriptase polymerase reaction, we have found that GEC and whole kidney expressed the C3 mRNA for C3. By ELISA, we have found that C3 was secreted in culture supernatants harvested from cultured GEC. The secretion of C3 is regulated by proinflammatory cytokines (IL-1 beta, TNF-alpha and IL-6). IL-1 beta is shown to be the most potent stimulator of C3 secretion from GEC. The exact significance of C3 produced at glomerular site is not clear, but its upregulation by proinflammatory cytokines may suspect a role in local activation of complement which may lead to glomerular injury. We further studied the expression of C3 step regulatory proteins (membrane cofactor protein (MCP), decay-accelerating factor (DAF), CR-1 and CD59 (a terminal step regulatory protein) by cultured GEC. Treatment of GEC by proinflammatory cytokines IL-1 beta, TGF-beta, TNF-alpha and IL-6 did not modify the expression of MCP, DAF and CR-1 whereas an increase in the expression of CD59 could be observed after treatment with IL-1 beta and TGF-beta. These results indicate that the expression of these regulatory proteins is tissue specific and may be implicated in inflammatory processes.
Nephron 1995
PMID:Human glomerular epithelial cells synthesize and secrete the third component of complement. 754 67

A previous study from our laboratory has shown that erythropoietin (EPO), beside its traditional role in erythropoiesis, acts as an alleviator of oxidative stress and inflammation in chronic hemodialysis (HD) patients, conferred in part by activated polymorphonuclear leukocytes (PMNLs). To substantiate this phenomenon, the existence of EPO receptors (EPO-Rs) on PMNL membrane was examined at the transcriptional and translational levels. mRNA for EPO-R was detected in PMNLs using specific primers directed towards the extracellular region of human EPO-R cDNA. The predicted 300-bp fragment was amplified by reverse transcriptase-polymerase chain reaction. Subcloning and sequence analysis revealed 100% homology of this fragment with human EPO-R. The receptor protein was detected on the surface of intact PMNLs using (125)I-EPO. The protein was further demonstrated by flow cytometric analysis using a fluorescent monoclonal anti-EPO-R. The percentage of PMNLs expressing EPO-R showed a strong correlation with the level of EPO in the serum, suggesting an upregulation of the receptor by the hormone. Taken together with our recent findings that EPO attenuates the oxidative stress and inflammation contributed by PMNLs in HD patients, the detection of functional EPO-R expression in PMNLs places these cells among the nonerythroid, EPO-responsive target populations.
Nephron 2001 Jul
PMID:The polymorphonuclear leukocyte--a new target for erythropoietin. 1142 50