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)

As some parts of human skin - such as genital and areolar skin - become pigmented after puberty, melanocytes in these regions are thought to be sex hormone target cells. We immunohistochemically localized androgen receptors in the nuclei of cultured human genital melanocytes by monoclonal and polyclonal antibodies. When these cells were incubated with [1,2-3H]-testosterone, the major metabolite in the medium was dihydrotestosterone and 5alpha-reduction predominated over 17beta-oxidation. Androgen receptor and type I 5alpha-reductase mRNAs could be detected in genital melanocytes by reverse transcriptase polymerase chain reaction. The tyrosinase activity was stimulated by the addition of androgen. This stimulation was antagonized by cyproterone acetate, whereas tyrosinase mRNA expression was not affected by androgen. These results indicate that human genital melanocytes are androgen target cells, and that androgen plays a role for pigmentation in the specific regional skin after puberty.
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PMID:Human genital melanocytes as androgen target cells. 932 83

Human immunodeficiency virus (HIV)-1 expression in mononuclear phagocytes is associated with multiple functional defects, including phagocytosis. To assess Fcgamma receptor (FcgammaR) function in cells expressing HIV-1, human promonocytic cells (U937) acutely or chronically infected with HIV-1, or stably transfected with a noninfectious reverse transcriptase (RT) defective HIV-1 provirus (Deltapol), were treated with phorbol 12-myristate 13-acetate for 48 hours and tested for their ability to ingest sheep erythrocytes coated with IgG (E-IgG). HIV-1-infected or transfected U937 cells ingested 50% to 65% fewer E-IgG than controls despite normal surface expression of FcgammaRs. HIV-1 specifically impaired FcgammaR-mediated phagocytosis, as ingestion of complement-coated erythrocytes was unaffected. U937 cells transfected with an env deficient mutant of HIV-1 ingested E-IgG normally, suggesting that the expression of HIV-1 env was required for HIV-1 to inhibit FcgammaR-mediated phagocytosis. Expression of HIV-1 in U937 cells was associated with an increased accumulation of intracellular cyclic adenosine monophosphate (cAMP); addition of the adenylate cyclase inhibitor 2',5'-dideoxyadenosine to these cells decreased intracellular cAMP levels to that of controls and restored FcgammaR-mediated phagocytosis. Addition of either interferon (IFN)-gamma or an inhibitor of cAMP-dependent protein kinase A (KT 5720) to HIV-1-transfected U937 cells also restored FcgammaR-mediated phagocytosis. Expression of HIV-1 induces a specific defect of FcgammaR function in mononuclear phagocytes that correlates with increased levels of cAMP, and can be corrected by pharmacologic manipulation.
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PMID:Human immunodeficiency virus-1 env impairs Fc receptor-mediated phagocytosis via a cyclic adenosine monophosphate-dependent mechanism. 934 63

Matrix metalloproteinase-1 (MMP-1) and tissue matrix metalloproteinase inhibitor 1 (TIMP-1) play an important role in remodeling the extracellular matrix in normal and pathological processes. The effect of phorbol-myristate acetate (PMA), interleukin-1 (IL-1), and tumor necrosis factor-alpha (TNF-alpha) on MMP-1 and TIMP-1 expression was studied on highly purified thyrocytes and undifferentiated 8505 C, C 643, HTh 74, SW 1736 thyroid carcinoma cells compared with thyroid-derived fibroblasts. Messenger RNA (mRNA) levels were monitored by competitive semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) after 24 hours. Culture supernatants were assayed for free and/or complexed MMP-1 and TIMP-1 after 48 hours using enzyme-linked immunosorbent assay (ELISA) systems (detection limit: <2 ng/mL). MMP-1 and TIMP-1 mRNA were present in all cell types, although thyrocytes showed MMP-1 mRNA levels near the detection limit. 8505 C expressed MMP-1 mRNA levels of up to 10(6) times those of the other cells analyzed. PMA and IL-1 increased MMP-1 mRNA in most cell types. TIMP-1 mRNA increased after treatment with PMA in all cells except 8505 C, whereas only slight effects were shown after IL-1 stimulation. MMP-1 protein was undetectable in normal thyrocyte cultures, but was secreted spontaneously by all cell lines ([ng/mL]; C 643: 15+/-7; HTh 74: 81+/-1; SW 1736: 13+/-2; 8505 C: 2097+/-320). There was a strong correlation between levels of MMP-1 mRNA and protein (r = 0.99, p < .0001). PMA and IL-1 increased MMP-1 secretion in all cell types after 48 hours. Fibroblasts ([ng/mL] 517+/-55) and the cell lines (C 643: 142+/-48; HTh 74: 115+/-13; SW 1736: 202+/-14; 8505C: 120+/-19) secreted TIMP-1 in unstimulated cultures, whereas only a trace amount was detected in thyrocyte cultures, even after PMA treatment. IL-1 upregulated TIMP-1 secretion after 48 hours in SW 1736, HTh 74, and C 643 cells. Our data suggest that in contrast to normal thyrocytes, dedifferentiated thyroid carcinoma cell lines are potential producers of MMP-1 as well as TIMP-1. High MMP-1 or MMP-1/TIMP-1 expression may play a role in tissue invasion of undifferentiated thyroid cancer cells.
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PMID:Human thyroid carcinoma cell lines and normal thyrocytes: expression and regulation of matrix metalloproteinase-1 and tissue matrix metalloproteinase inhibitor-1 messenger-RNA and protein. 934 74

Tissue factor (TF) is a main initiator of the coagulation protease cascade. Control of the expression of this protein in monocytes is essential, since these cells are the only circulating blood cells responsible for TF expression. In this report we have used two human cell lines, arrested at different stages of monocytic differentiation, to study TF expression. The monoblastic cell line U-937 had a constitutive expression of TF surface protein and low TF mRNA levels detected by immunofluorescence or quantitative reverse transcriptase polymerase chain reaction respectively. The phorbol-12-myristate-13-acetate (PMA) was a potent enhancer of TF expression in U-937. Lipopolysaccharide (LPS) and tumor necrosis factor (TNF) had no effect on TF expression in U-937. The Mono Mac 6 cell line, with phenotypic features similar to that of mature monocytes, expressed lower basal levels of TF mRNA and surface TF antigen. However, in Mono Mac 6 cells TF expression was induced in response to LPS and TNF. These results indicate differences in basal and induced TF expression between U-937 and Mono Mac 6 cell lines.
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PMID:Tissue factor expression in human monocytic cell lines. 936 74

Growth hormone (GH) is produced in progestin-induced hyperplastic ductular mammary epithelia in dogs. Progestins also induce the development of cystic endometrial hyperplasia (CEH) in this species. The study reported here investigated whether GH gene expression could also be demonstrated in progestin-induced hyperplastic epithelium in the canine uterus. Eight beagle bitches were treated with 10 mg medroxyprogesterone acetate (MPA) kg-1 body mass s.c. at intervals of 3 weeks, for a total of five times in four dogs (group I) and for a total of 13 times in the other four dogs (group II). Blood samples were collected twice during each 3 week period for measurement of plasma concentrations of GH, insulin-like growth factor I (IGF-I) and IGF-II. At the end of the series of injections uterine tissue was obtained by ovario-hysterectomy. Histological examination confirmed that CEH was present in all uteri after MPA treatment; the changes in the dogs of group I were less marked than those in group II. Immunohistochemical examination of the uterine tissues showed that immunoreactive(i) GH was present in a number of uteri with CEH. iGH was usually located in the cytoplasm of glandular epithelial cells. However, reverse transcriptase PCR using GH-specific primers failed to demonstrate mRNA encoding GH in the uterine tissue of all dogs. It is concluded that local production of GH is not involved in progestin-induced hyperplasia of uterine epithelial cells in dogs.
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PMID:Lack of association of progestin-induced cystic endometrial hyperplasia with GH gene expression in the canine uterus. 940 6

Platelet-activating factor (PAF) has been implicated in the pathogenesis of allergic and inflammatory events in the airway. In the present study, we sought to determine if PAF receptors are present on human bronchial epithelial cells and whether PAF binding to these receptors leads to activation of activator protein-1 (AP-1)-mediated transcription. Radioligand binding studies demonstrated specific binding sites for the PAF antagonist [3H]WEB 2086 (3-[4-(2-chlorophenyl)-9-methyl-6H-thieno[3,2-f]-[1,2,4]triazolo[4,3- a][1,4]diazepine-2-yl]-1-(4-morpholinyl)-1-propanone) on primary bronchial epithelial cells with an equilibrium dissociation constant (Kd) = 9.8 nM and maximal density of binding sites (Bmax) = 42.4 fmol/mg of protein. The expression of PAF receptors in these cells was further confirmed by reverse transcriptase-polymerase chain reaction, which revealed amplification products derived from PAF receptor mRNA corresponding to transcripts 1 and 2. In the bronchial epithelial cell line BEAS-2B transfected with an expression plasmid for the human PAF receptor, PAF stimulation increased AP-1 DNA binding activity as determined by electrophoretic mobility shift assays. The Fos and Jun family proteins were identified as components of the DNA-protein complexes by anti-peptide antibodies in gel supershift assays. Additionally, PAF significantly induced AP-1 mediated transcription which was dependent on the expression of PAF receptors. The PAF antagonist WEB 2086 blocked the PAF effect but not that induced by 12-O-tetradecanoyl phorbol-13-acetate, indicating the specificity of the PAF response. These results indicate that activation of airway epithelial cells through stimulation of PAF receptors includes up-regulation of the nuclear transcription factor AP-1 and AP-1 transcriptional activity.
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PMID:Platelet-activating factor induction of activator protein-1 signaling in bronchial epithelial cells. 944 41

Thyroid cancer can degrade basement membranes and invade tissues. This depends on a cascade of matrix metalloproteinases involving membrane-type 1 matrix metalloproteinase (MT1-MMP), MMP-2, and MMP-9. We analyzed the expression and role of these MMPs and their specific inhibitors TIMP-2 and TIMP-3 in human highly purified thyroid epithelial, C 643, HTh 74, SW 1736, and 8505 C thyroid carcinoma and thyroid-derived fibroblast cell cultures. The effect of phorbol-myristate acetate (PMA), and of the inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) on MMP and TIMP mRNA levels were monitored by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) including an internal homologous competitor fragment. The highest MT1-MMP mRNA levels were found in thyroid-derived fibroblasts. The MT1-MMP mRNA expression was increased up to 10-fold by PMA, while all other growth factors tested had only negligible effects. The thyroid carcinoma cells themselves did not seem to play a crucial role in the production of MT1-MMP in thyroid tumors. Higher MMP-2 mRNA levels were found in all cell types investigated. The highest MMP-2 mRNA levels were determined in thyroid-derived fibroblasts and HTh 74 cells. We found a lack of MMP-2 response to IL-1, TNF-alpha, and phorbol esters. In unstimulated cells, MMP-9 mRNA was found near the detection limit or at low levels. In nearly all cell types, treatment with PMA, IL-1, and TNF-alpha caused an increase of the MMP-9 mRNA levels. The results of basal and stimulated MMP-2 and MMP-9 mRNA expression were confirmed at the protein level by gelatin zymography. TIMP-2 and TIMP-3 mRNAs were expressed at high levels. In contrast to the basal TIMP-3 mRNA levels, which varied over a great range, there were no striking differences the cell types from analyzing TIMP-2 mRNA. There were no or only slight stimulatory effects on TIMP-2 and TIMP-3 mRNA expression by IL-1, TNF-alpha, and PMA. Taken together, most enzymes of the MT-MMP/MMP class of proteases facilitating invasion of thyroid tumor cells seem to have been produced by fibroblasts, not by the tumor cells themselves. However, some dedifferentiated thyroid tumor cell lines may be capable of secreting some of these enzymes, as in the case of HTh 74 cells.
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PMID:mRNA levels of membrane-type 1 matrix metalloproteinase (MT1-MMP), MMP-2, and MMP-9 and of their inhibitors TIMP-2 and TIMP-3 in normal thyrocytes and thyroid carcinoma cell lines. 954 6

Malignant rhabdoid tumors (MRT) are characterized by unique neoplastic cells demonstrating phenotypic diversity. By using the reverse transcriptase-polymerase chain reaction, we have detected expression of various genes before and after differentiation induction with four different agents in four established MRT cell lines (TM87-16, STM91-01, TTC642, and TTC549). The agents used in this study were all-trans retinoic acid (RA), 12-O-tetradecanoylphorbol-13-acetate (TPA), interleukin-3, or interferon-gamma. Before and after induction, c-myc, IGF-II, IGF-I receptor, and IGF-II receptor were constitutively expressed by all four cell lines. The neurofilament medium-size (NF-M) was constitutively expressed by the TM87-16 and TTC642, and the S100 protein alpha subunit was expressed by TM87-16, TTC642, and TTC549. Chromogranin A was expressed by TM87-16 only after treatment with either TPA or RA. MyoD, N-myc, tyrosine hydroxylase, N-CAM, trkA, and the S100 protein beta subunit were not expressed by any cell line before or after induction with these agents. All the MRT cell lines in this study except TM87-16 were highly resistant to differentiation induction. The proliferating cells in TM87-16 and TTC642 expressed mRNA profiles characteristic of neuroectoderm.
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PMID:Gene expression of malignant rhabdoid tumor cell lines by reverse transcriptase-polymerase chain reaction. 955 92

Phytohaemagglutinin stimulates lymphoid cells to initiate active cell division which is tightly coordinated with transcription of ribosomal RNA genes. Nuclear Run-On assays demonstrated that treatment of peripheral blood lymphocytes with PHA (10 microg/ml) resulted in maximal rRNA synthesis after 64 hrs. In contrast, mRNA levels for upstream binding factor (UBF)1 and UBF2, as measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and Southern blotting, increased relatively rapidly within 3 to 6 hrs. and remained elevated for at least the next 60 hrs. We further showed that exponentially growing cells of promyelocytic leukemia line HL-60 contained the same amounts of UBF1 and UBF2 mRNAs as phytohaemagglutinin (PHA)-stimulated lymphocytes for 6 hrs. Growth arrest of HL-60 cells, caused by 10 nM phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced monocytic/macrophage-like differentiation for 72 hrs., has been accompanied by a 50% decrease in UBF1/2 mRNAs expression. The lowest concentrations of UBF1/2 mRNAs were revealed in non-dividing terminally differentiated granulocytes. Regardless the activity of RNA polymerase I transcription and cell division rate, UBF1 mRNA levels prevailed over UBF2 mRNA levels in all human blood cell populations tested. Our results suggest that UBF gene expression is an important regulatory mechanism involved in the acceleration and possibly deceleration of rDNA transcription observed during mitogenic stimulation and inhibition of blood cells.
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PMID:Early gene expression of both RNA polymerase I transcription factors UBF1 and UBF2 precedes ribosomal RNA synthesis during lymphocyte mitogenic stimulation. 959 85

The products of the human Arg gene and human, mouse, Drosophila, and nematode Abl genes characterize the Abelson family of nonreceptor tyrosine protein kinase. The Arg gene, expressed as a 12-kb transcript, codes a protein highly related to c-abl in the tyrosine kinase, SH2, and SH3 domains, and both proteins have a myristoylated isoform. The C-terminal domains of Arg and c-abl, poorly similar to each other, may account for their different functions. Arg is cytoplasmic, c-abl also has nuclear localization, and their products have different transforming activity. To gain insight about the role of Arg in myeloid differentiation we investigated Arg gene expression in HL-60 cells differentiated with all-trans retinoic acid and 12-O-tetradecanoyl-phorbol-13-acetate. With a semiquantitative reverse transcriptase-polymerase chain reaction assay it was evident that the Arg transcript level in HL-60 cells differentiated toward granulocyte and macrophage-like lineage was, respectively, 3.5- and 2.8-fold the Arg level evidenced in undifferentiated HL-60 cells. In the HL-60 cells, under the same differentiating conditions, the c-abl RNA level did not change significantly, showing that Arg and c-abl responded in a different way to the inducers of differentiation used.
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PMID:Increment of nonreceptor tyrosine kinase Arg RNA as evaluated by semiquantitative RT-PCR in granulocyte and macrophage-like differentiation of HL-60 cells. 982 10


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