Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

We investigated the cell toxicity of polychlorinated biphenyls (PCBs) and 2,3,4,7,8-pentachlorodibenzofuran (PCDF) as an indicator of the quantity of m-RNA, which synthesizes the HBV core antigen region, and secreting protein, which is an HBV surface antigen in PLC/PRF/5 cells. The determination of m-RNA was conducted according to the methods of reverse transcriptase and polymerase chain reaction. Furthermore, the reductive action of ursodeoxycholic acid, shou-saiko-to and inchin-gorei-san on the PCBs and PCDF toxicity was investigated. The cell number of 1 x 10(5)/ml and concentrations of 200 micrograms/ml for PCBs and 500 microM for PCDF were used in these experiments. The titer of HBsAg was gradually increased from 1 in 1 x 10(3)/ml of cell numbers to 100 in 1 x 10(6)/ml of cell numbers. The curve became a plateau in 1 x 10(6)/ml of cell numbers. The cell number of 1 x 10(5)/ml was used in the experiments. The titer of HBsAg decreased following in the increase of concentration of PCBs. The HBsAg, even in the PCBs concentration of 1000 micrograms/ml showed a titer of 22.5%. However, the highest concentration of PCDF in this study, that is, 500 microM of PCDF, did not show any decrease of HBsAg activity. The concentrations of 200 micrograms/ml for PCBs and 500 microM for PCDF were used in the investigation of drug effects. A high titer HBsAg was observed in high concentrations of shou-saiko-to in comparison with a control group. Ursodeoxycholic acid and inchin-gorei-san exhibited a similar tendency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vitro analysis of polychlorinated biphenyls (PCBs) and 2,3,4,7,8-pentachlorodibenzofuran (PCDF) cellular toxicity in PLC/PRF/5 cell proliferation--the effect of ursodeoxycholic acid, inchin-gorei-san and shou-saiko-to on cell toxicity. 191 93

In previous reports, the authors demonstrated that M-CSF was produced by primary-cultured non-parenchymal (NPLC) and parenchymal (PLC) liver cells. In order to clarify the biological role of M-CSF produced by the liver, macrophage colony-stimulating factor (M-CSF)-producing cells in vivo were investigated using reverse transcriptase polymerase chain reaction (RT-PCR), dot blot analysis, in situ hybridization and immunohistochemistry. M-CSF mRNA was constantly identified by RT-PCR in the liver, NPLC and PLC, before and after partial hepatectomy. Dot blot analysis showed that fluctuations of M-CSF mRNA level after partial hepatectomy were not statistically significant. In situ hybridization revealed that M-CSF mRNA was expressed mainly in NPLC and vascular endothelial cells (VEC). In addition, a small number of PLC also expressed M-CSF mRNA. Neither the distribution nor the frequency of M-CSF mRNA positive cells in regenerative livers differed significantly from normal livers. M-CSF immunoreactivity was present in NPLC and VEC at all the times before and after partial hepatectomy, while PLC exhibited M-CSF immunostaining 0.5 days after partial hepatectomy. As normal liver expressed M-CSF mRNA to the same degree as regenerative liver, hepatic M-CSF mRNA production in vivo may be related to the physiological function of the liver. However, transient expression of M-CSF protein in PLC at an early stage after partial hepatectomy may be associated with liver regeneration.
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PMID:Production of macrophage colony-stimulating factor by murine liver in vivo. 906 96

The cytokeratin 18 related molecules of human hepatocellular carcinoma have been previously recognized through a series of biochemical and immunological approaches. It is suggested that these molecules undergo modulation from human hepatocyte cytokeratin 18. To prove whether these molecules are produced by modulation or protein degradation, we checked the cytokeratin profile of human hepatoma cell line PLC/PRF/5 with the methods used before. These results revealed that the PLC cells have the same cytokeratin 18 related molecules as human hepatocellular carcinoma tissue. The gene expression of the cytokeratin 18 in non-tumor liver tissues, hepatocellular carcinoma and PLC/PRF/5 cells were investigated. First, the mRNAs of non-tumor liver tissues, hepatocellular carcinoma tissues and PLC/PRF/5 cells were collected by the acid guanidinium thiocyanate phenol chloroform method. After transcription into cDNA by reverse transcriptase polymerase chain reaction, the cDNAs of each specimen were amplified by PCR and then digested by SmaI and BamHI restriction enzymes. The digested cDNA fragments were electrophoresed in agarose gel and the base pairs were found to be the same in length between neoplastic and non-neoplastic hepatocytes.
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PMID:The alteration of cytokeratin 18 molecule and its mRNA expression during tumor transformation in hepatoma. 926 84

We previously reported that there is a developmental increase in surfactant secretion in response to P2Y2 purinoceptor agonists. UTP does not stimulate secretion in type II cells from 1- or 2-day-old rats; there is a small response to UTP in cells from 4-day-old animals, and the response increases with increasing age thereafter. Second messenger formation in response to P2Y2 agonists has a similar developmental pattern. We have investigated whether the failure to respond to P2Y2 agonists is due to a deficiency in the P2Y2 receptor or in downstream signaling factors. We compared type II cells from adult and 1- to 2-day-old rats with respect to expression of the P2Y2 receptor gene and the levels of phospholipase C-beta (PLC-beta) and protein kinase C (PKC) isomers and of the alpha-subunit of the GTP-binding protein Gq. We measured gene expression by reverse transcriptase-polymerase chain reaction and protein levels by immunoblotting. We identified PKC-alpha, -betaI, -betaII, -delta, -eta, -zeta, -theta, and -mu, PLC-beta3, and Gqalpha in adult and newborn type II cells. PKC-epsilon, -gamma, and -lambda and PLC-beta1, -beta2, and -beta4 were not present in adult or newborn type II cells. Expression of the P2Y2 receptor gene was essentially the same in newborn and adult cells. However, the levels of PKC-alpha, -betaI, -betaII, and -zeta in newborn type II cells were only 43-57% those of adult cells. The level of PKC-theta also tended to be lower in the newborn cells. There was little difference between newborn and adult type II cells in the levels of PKC-delta, -eta, and -mu, PLC-beta3, and Gqalpha. These data suggest that the lack of response of early newborn type II cells to P2Y2 agonists is not due to a lack of expression of the receptor gene but possibly to insufficient amounts of one or more of the alpha, betaI, betaII, or zeta PKC isoforms.
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PMID:PKC isoforms and other signaling proteins involved in surfactant secretion in developing rat type II cells. 960 28

Nevirapine (NVP) is a nonnucleoside reverse transcriptase inhibitor widely used in combination with other antiretroviral agents for the treatment of human immunodeficiency virus disease. To establish its safety profile, we conducted a review of data from prospective US and international clinical trials involving a total of 906 adult patients and 468 pediatric patients treated with NVP. Drug-related adverse events were similar in adults and children, with rash and nausea most frequently reported in adults and rash and granulocytopenia most frequently reported in children. A separate analysis of rash based on data from adult patients in controlled trials demonstrated a 16% rate of NVP-attributable rash in these patients. Of patients with NVP-associated rash, 65% developed rash within the first 6 weeks of therapy, and it has been shown that a lower lead-in dose (200 mg/d vs the standard 400 mg/d) for the first 2 weeks of NVP treatment reduces the frequency of drug-associated rash. Serious rash (Stevens-Johnson syndrome [SJS] or SJS/toxic epidermal necrolysis transition syndrome) occurred with an incidence of 0.3% and clinical hepatitis with an incidence of 1.0% among NVP-treated patients in clinical trials. Adverse event data from long-term clinical trials demonstrated a lower incidence of NVP-related adverse events than in short-term trials of NVP therapy. An analysis of abnormal laboratory findings using thresholds similar to those found in the prescribing information for other commonly used antiretroviral agents and data from controlled trials in adults showed that the most frequently observed laboratory abnormalities were elevations in liver function test results. Approximately 50,000 patients in the United States had been treated with marketed NVP at the time of writing, and postmarketing surveillance has supported the overall safety profile observed in clinical trials. NVP has been shown to be well tolerated in both adult and pediatric patients.
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PMID:Safety profile of nevirapine, a nonnucleoside reverse transcriptase inhibitor for the treatment of human immunodeficiency virus infection. 991 3

This study examined the expression of the platelet collagen receptor glycoprotein VI (GPVI) in megakaryocyte cell lines and primary megakaryocytes by reverse transcriptase-polymerase chain reaction and by flow cytometry and ligand blotting using the snake venom toxin convulxin. Expression of GPVI is increased in the megakaryoblastic cell lines HEL and CMK on differentiation with the phorbol ester phorbol 12-myristate 13-acetate (PMA), along with the Fc receptor gamma-chain (FcR gamma-chain). The increase in GPVI expression is associated with marked potentiation of tyrosine phosphorylation and Ca(++) elevation in response to convulxin. Syk, linker for activated T cells, and phospholipase C gamma 2 (PLC gamma 2) are among the proteins tyrosine phosphorylated on convulxin stimulation in PMA-differentiated HEL cells. Studies on primary murine megakaryocytes grown in vitro confirmed that GPVI is up-regulated in parallel with functional activation, assessed by measurement of [Ca(++)](i), during differentiation. The results demonstrate that expression of GPVI is up-regulated along with the FcR gamma-chain during differentiation of megakaryocytes. (Blood. 2000;96:2740-2745)
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PMID:Expression of the collagen receptor glycoprotein VI during megakaryocyte differentiation. 1102 7

This study examined, in human cancer lines, the pattern of cytokine production stimulated by lipopolysaccharide (LPS), a major component of outer surface of gram-negative bacteria, and characterized the expression pattern of CD14, cell surface LPS receptor antigen, and toll-like receptors (TLRs), which appear to be key regulators of the innate immune response system. Two colon cancer cell lines (DLD and LoVo), a hepatocellular carcinoma cell line and a myelomonocytic cell line were incubated with LPS for 0-72 h, and transforming growth factor (TGF) beta1 and beta2, hepatocyte growth factor (HGF) and interleukins 6, 8 and 15 were assayed. The only changes induced by incubation with LPS were significant increases in TGFbeta1 production at 12 h, and in HGF production at 72 h, in LPS-stimulated DLD cells, and significant increases in TGFbeta2 production after 12 h and in HGF after 72 h in LoVo cells. Using reverse transcriptase-polymerase chain reaction analysis, expression of CD14 and TLR-2 mRNA was detected in DLD and LoVo cells, and expression of TLR-4 mRNA was detected in PLC/PRF/5 and KG-1 cells. These results suggest that LPS induces TGFbeta and HGF production mediated by CD14/TLR-2 in cultured human colon cancer cell lines.
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PMID:Bacterial lipopolysaccharide induces transforming growth factor beta and hepatocyte growth factor through toll-like receptor 2 in cultured human colon cancer cells. 1172 28

We have previously isolated and characterized a novel human gene HUEL (C4orf1) that is ubiquitously expressed in a wide range of human fetal, adult tissues and cancer cell lines. HUEL maps to region 4p12-p13 within the short arm of chromosome 4 whose deletion is frequently associated with bladder and other carcinomas. Here we present the genomic organization, sizes and boundaries of exons and introns of HUEL. The GC-rich upstream genomic region and 5' untranslated region (UTR) together constitute a CpG island, a hallmark of housekeeping genes. The 3250 bp HUEL cDNA incorporates a 1704 bp ORF that translates into a hydrophilic protein of 568-amino acids (aa), detected as a band of approximately 70 kDa by Western blotting. We have isolated the murine homolog of HUEL which exhibits 89% nucleotide and 94% amino acid identity to its human counterpart. The HUEL protein shares significant homology with the minimal DNA-binding domain (DNA-BD) of the DNA repair protein encoded by the xeroderma pigmentosum group A (XPA) gene. Other notable features within HUEL include the putative nuclear receptor interaction motif, nuclear localization and export signals, zinc finger, leucine zipper and acidic domains. Mimosine-mediated cell cycle synchronization of PLC/PRF/5 liver cancer cells clearly portrayed translocation of HUEL into the nucleus specifically during the S phase of the cell cycle. Yeast two-hybrid experiments revealed interactions of HUEL with two partner proteins (designated HIPC and HIPB) bearing similarity to a mitotically phosphorylated protein and to reverse transcriptase. Co-immunoprecipitation assays validated the interaction between HUEL and HIPC proteins in mammalian cells. HUEL is likely to be an evolutionarily conserved, housekeeping gene that plays a role intimately linked with cellular replication, DNA synthesis and/or transcriptional regulation.
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PMID:The novel human HUEL (C4orf1) protein shares homology with the DNA-binding domain of the XPA DNA repair protein and displays nuclear translocation in a cell cycle-dependent manner. 1190 20

Aminoglycoside antibiotics (AGAs) are nephrotoxic, with most of the damage confined to the proximal tubule, but the mechanism for cellular toxicity is not clear. It has been previously shown that the extracellular-calcium sensing receptor (CaR) is expressed in intact rat proximal tubule and can be stimulated by the AGA neomycin. To investigate whether CaR could contribute to AGA-induced nephrotoxicity, the acute responses to various AGAs in the proximal tubule-derived opossum kidney (OK) cell line were examined. The presence in OK cells of CaR-related transcripts and protein was demonstrated by northern analyses, reverse transcriptase-PCR, immunocytochemistry, and immunoblotting. OK cells responded to elevated extracellular calcium (Ca(2+)(o)) and neomycin but also to gentamicin and tobramycin with an increase in cytosolic [Ca(2+)]. Ca(2+)(o), neomycin, and gentamicin also activated the extracellular signal-regulated kinases, ERK1 and ERK2. Neomycin-induced ERK activation was both dose- and time-dependent and was attenuated by inhibitors of phosphatidylinositol 3-kinase, phosphatidylinositol bisphosphate (PIP(2))-specific phospholipase C, and MEK1, but not of protein kinase C. Thus, proximal tubular OK cells express a CaR that mediates Ca(2+)(i) mobilization and PIP(2)-PLC-dependent ERK activation in response to AGAs and thus could play a role in AGA-induced nephrotoxicity.
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PMID:Aminoglycosides increase intracellular calcium levels and ERK activity in proximal tubular OK cells expressing the extracellular calcium-sensing receptor. 1203 77

To identify the genes responsible for carcinogenesis and progression of hepatocellular carcinoma (HCC), we screened differentially expressed genes in several human HCC cell lines. Among these genes, Gpr49 was up-regulated in PLC/PRF/5 and HepG2. Gpr49 is a member of the glycoprotein hormone receptor subfamily, which includes the thyroid-stimulating hormone receptor (TSHR). However, Gpr49 remains to be an orphan G-protein-coupled receptor. By real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR) analysis, overexpression (>3-fold increase compared with the corresponding noncancerous liver tissue) of Gpr49 mRNA was observed in 18 of 38 (47%) HCCs compared with corresponding noncancerous livers. Clinicopathologically, overexpression of Gpr49 was frequently observed in HCC with mutation in beta-catenin exon 3 (14 of 16 cases, 87.5%). Moreover, introduction of mutant beta-catenin into mouse hepatocytes in culture caused up-regulation of the Gpr49 mouse homologue. Therefore, Gpr49 is likely to be a target gene activated by Wnt-signaling in HCC. In conclusion, although much is still unknown, Gpr49 may be critically involved in the development of HCCs with beta-catenin mutations and has the potential to be a new therapeutic target in the treatment of HCC.
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PMID:Overexpression of orphan G-protein-coupled receptor, Gpr49, in human hepatocellular carcinomas with beta-catenin mutations. 1260 49


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