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)

The mouse adrenocortical Y-1 cell line expresses a high level of neuropeptide Y1 receptor (NPY-Y1). Moreover the receptor density can be up-regulated by dexamethasone or down-regulated by cAMP. To determine whether such regulation occurs at the level of gene expression, Y1 receptor mRNA was measured using a reverse transcriptase-competitive PCR method. Dexamethasone treatment increased Y1 mRNA in Y-1 cells, whereas the cAMP and ACTH decreased it. We also observed that the amount of Y1 receptor RNA was unaffected by phorbol 12-myristate 13-acetate, a protein kinase C stimulator, but was abolished in a cell line expressing apolipoprotein E (apoE). The results indicated that NPY-Y1 receptor mRNA in Y-1 cells is highly regulated by several intracellular messengers. The role of apoE in such regulation is of particular interest in view of evidence that the isoform of the molecule is highly correlated to the age of onset of Alzheimer's disease. The effect observed in the Y-1 cell line which expresses apoE may implicate a possible role of this protein in the process of neuronal death that occurred in the Alzheimer's disease.
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PMID:Neuropeptide Y receptor gene regulation in mouse adrenocortical Y-1 cells. 879 89

Nerve growth factor (NGF) is of major importance for the survival, development and maintenance of peripheral sympathetic and central neuronal tissue. Most of the cellular effects are mediated by binding to their high-affinity receptor c-TRK, a transmembrane receptor tyrosine kinase. C-TRK protein has been detected in neuronal tissue and also in mast cells, monocytes and some haemopoletic progenitor cells. Here we report c-TRK gene expression in myeloid leukaemic cell lines (HEL, K562 and KG-1) and for the first time in the primary leukaemic cells of 44% (n = 59) of patients with acute myelogenous leukaemia (AML). Moreover, in the human promyelocytic cell line HL-60, c-TRK expression was inducible by differentiation induction with tetradecanoyl-phorbol 13-acetate (TPA). In c-TRK gene-expressing cells the transmembrane receptor tyrosine kinase was detectable by Western blotting and by in vitro kinase assay. In the AML group, c-TRK expression was not correlated to the FAB-classified morphology or any other clinical parameter. In all cases tested we could not detect NGF mRNA by means of reverse transcriptase PCR, excluding an autocrine loop involving the TRK/NGF receptor-ligand system in leukaemogenesis. Our results show another example of possible communication between neuronal and haemopoietic tissue. However, we still lack positive evidence of a c-TRK function in haemopoiesis.
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PMID:Expression of the nerve growth factor receptor c-TRK in human myeloid leukaemia cells. 885 45

Using reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), we studied the generation of the recently described Th2 cytokine interleukin-13 (IL-13) by anti-IgE-activated lung fragments (LF), lung mast cells (LMC), and the mast cell line HMC-1. We found that IL-13 messenger ribonucleic acid (mRNA) was constitutively expressed in LF and rapidly increased after anti-IgE challenge, persisting throughout a 16-h period. Quantitative-competitive PCR (QCPCR) demonstrated an increase from 1.2 fg to 120 fg of IL-13 mRNA/micrograms LF total cellular RNA. Time-course experiments showed that IL-13 protein was not increased in supernatants at 2 h after activation, but was upregulated by 8 h. Anti-IgE-activated LF supernatants contained 592.1 +/- 314.8 pg IL-13/g wet weight of tissue at 24 h (mean +/- SE; n = 11). LMC demonstrated upregulation of IL-13 mRNA expression following treatment with A23187 (n = 4), with maximal upregulation by 3 h; anti-IgE or phorbol myristate acetate (PMA) also led to increased IL-13 mRNA expression. QCPCR analysis of LMC IL-13 mRNA expression at 4 h after activation showed a 7-, 13.8-, and 13.2-fold increase after A23187, anti-IgE, and PMA, respectively. Quantities of IL-13 released from optimally activated LMC and peripheral blood T cells were comparable. HMC-1 also showed enhanced IL-13 mRNA beginning 30 min after A23187 activation, with peak expression from 1 to 10 h, followed by waning over the subsequent 24 h. A23187 stimulation of HMC-1 led to 100-fold upregulation of IL-13 mRNA within 4 h and detectable IL-13 in 24-h supernatants. These results demonstrate that activation of LF and LMC through multiple signal-transduction pathways results in increased IL-13 mRNA and protein expression temporally consistent with a potential role in chronic allergic inflammation.
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PMID:Human lung mast cell activation leads to IL-13 mRNA expression and protein release. 887 81

Tumour necrosis factor "alpha" (TNF "alpha") is a pleiotropic cytokine that is produced mainly by monocytes and macrophages. TNF "alpha" appears to be responsible for many of the inflammatory and necrotic changes seen in malignant or infectious liver diseases. In addition, blood levels of TNF "alpha" have been reported to be elevated in those with hepatic diseases. Although TNF "alpha" is synthesized mainly by monocytes and macrophages, its production has recently been found in nonhaemopoietic cells as well. Therefore we have used the human liver cell line HepG2 to test for the inducible production of TNF "alpha" in hepatic parenchymal cells. No constitutive TNF "alpha" gene expression was detected by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). However, treatment with the proinflammatory cytokine interleukin 1 "beta" (IL-1 "beta") or phorbol 12-myristate-acetate (PMA) led to a marked increase in TNF "alpha" mRNA levels. Maximal TNF "alpha" mRNA levels were observed after 3-h incubation periods, decreased thereafter and became undetectable after 12 h. The culture supernatant from cells treated with IL-1 "beta" or PMA contained significant amounts of TNF "alpha" protein which was immunologically detectable and biologically active. We believe that our report of inducible TNF "alpha" production in this widely available hepatic cell line adds a valuable tool for understanding TNF "alpha" gene expression in nonhaematopoietic cells.
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PMID:Interleukin 1 beta and phorbol ester induce tumour necrosis factor alpha production in a hepatic cell line (HepG2). 892 10

Cell cycle progression requires activation of different cyclin-dependent kinases (CDKs) which are positively regulated by cyclins and negatively regulated by CDK inhibitors. Growth inhibition of the Calu-1 lung carcinoma cells induced with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), a potent activator of protein kinase C, is associated with G2/M arrest and induction of expression of a novel, faster-migrating form of p21(WAF1/CIP1/SDI1) (p21) protein, an inhibitor of cyclin-dependent kinases. This faster-migrating p21 protein was also expressed in TPA-treated A549 lung carcinoma cells which also exhibited G2/M arrest but not in TPA-treated U937 leukemia cells, which only expressed a slower-migrating form of p21 protein. However, reverse transcriptase-polymerase chain reaction and Southern analysis demonstrated no evidence of novel splice in TPA-treated Calu-1 cells. On the other hand, immunoblotting analysis demonstrated that the faster-migrating p21 protein could be detected only by peptide antibody directed against the N terminus but not the C terminus, suggestive of truncation of the latter or protein modification that results in the loss of the C-terminal epitope. Correlation of G2/M arrest with expression of the faster-migrating p21 protein suggests that this novel form of p21 protein may be a mediator of G2/M arrest and growth inhibition.
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PMID:Novel form of p21(WAF1/CIP1/SDI1) protein in phorbol ester-induced G2/M arrest. 893 83

Prostatic growth occurs through ductal elongation and branching into the mesenchyme. Ductal branching morphogenesis in the prostate is elicited by androgens via mesenchymal-epithelial interactions mediated by paracrine influences from mesenchyme. The role of keratinocyte growth factor (KGF) was investigated in the developing prostate as KGF has been suggested to be a paracrine acting factor. KGF transcripts were detected by reverse transcriptase-polymerase chain reaction (RT-PCR) in neonatal rat ventral prostates (VPs) in vivo, in VPs cultured in vitro, and in isolated VP mesenchyme. KGF receptor was detected in VP's by RT-PCR and was localized specifically to the epithelium by in situ hybridization. KGF was investigated as a potential paracrine mediator during androgen-induced prostatic development by examining neonatal rat VPs cultured for 6 days under serum-free conditions using a basal medium supplemented only with insulin and transferrin. When testosterone (10(-9) to 10(-8) M) was added to the basal medium, VPs grew and underwent ductal branching morphogenesis similar to that in situ. Neutralization of endogenous KGF with a monoclonal antibody to KGF (anti-KGF) or a soluble KGF receptor peptide inhibited androgen-stimulated VP growth (DNA content) and reduced the number of ductal end buds after 6 days of culture. When KGF (50 or 100 ng/ml) was added to the basal medium in the absence of testosterone, VP growth and ductal branching morphogenesis were stimulated. The number of ductal end buds was about 70% of that obtained with an optimal dose of testosterone (10(-8)M), and DNA content of VP's cultured with 100 ng/ml KGF was equivalent to that of glands cultured with testosterone. The stimulatory effect of KGF was partially blocked by cyproterone acetate, a steroidal anti-androgen. These data imply that KGF plays an important role as a mesenchymal paracrine mediator of androgen-induced epithelial growth and ductal branching morphogenesis in the rat VP.
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PMID:Keratinocyte growth factor (KGF) can replace testosterone in the ductal branching morphogenesis of the rat ventral prostate. 894 42

PGF2 alpha is a metabolite of arachidonic acid that triggers regression of the corpus luteum. Recent animal studies have indicated that PGF2 alpha (FP) receptor messenger ribonucleic acid (mRNA) is expressed in the corpus luteum. To understand the regulation of the FP receptor in the ovary we have cloned a partial complementary DNA (cDNA) sequence of the FP receptor from human granulosa cells obtained from women undergoing in vitro fertilization. The sequence of this cDNA is identical to the previously reported FP receptor sequences obtained from human uterine and placental cDNA libraries. Low levels of the FP receptor mRNA were observed in freshly isolated granulosa cells or in cultured granulosa-luteal (GL) cells, as detected by reverse transcriptase-PCR. hCG and 8-bromo-cAMP increased the steady state levels of the FP receptor mRNAs after incubation for 24-48 h, as detected by Northern blot hybridization. The stimulatory effect of hCG was concentration and culture stage dependent. Further, hCG and 8-bromo-cAMP increased binding of radiolabeled PGF2 alpha to intact GL cells. In contrast, phorbol 12-myristate 13-acetate inhibited basal as well as hCG- and 8-bromo-cAMP-induced FP receptor mRNA expression and binding of the radiolabeled ligand. In summary, hCG, 8-bromo-cAMP, and phorbol 12-myristate 13-acetate modulate the expression of the FP receptor in human GL cells, which may represent a mechanism to regulate the responsiveness of the ovary to PGF2 alpha.
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PMID:Regulation of prostaglandin F2 alpha receptor expression in cultured human granulosa-luteal cells. 897 3

We reported earlier that the levels of Ca2+-dependent metalloproteinases are increased in Alzheimer's disease (AD) specimens, relative to control specimens. Here we show that these enzymes are forms of the matrix metalloproteinase MMP-9 (EC3.4.24. 35) and are expressed in the human hippocampus. Affinity-purified antibodies to MMP-9 labeled pyramidal neurons, but not granular neurons or glial cells. MMP-9 mRNA is expressed in pyramidal neurons, as determined with digoxigenin-labeled MMP-9 riboprobes, and the presence of this mRNA is confirmed with reverse transcriptase PCR. The cellular distribution of MMP-9 is altered in AD because 76% of the total 100 kDa enzyme activity is found in the soluble fraction of control specimens, whereas only 51% is detectable in the same fraction from AD specimens. The accumulated 100 kDa enzyme from AD brain is latent and can be converted to an active form with aminophenylmercuric acetate. MMP-9 also is detected in close proximity to extracellular amyloid plaques. Because a major constituent of plaques is the 4 kDa beta-amyloid peptide, synthetic Abeta1-40 was incubated with activated MMP-9. The enzyme cleaves the peptide at several sites, predominantly at Leu34-Met35 within the membrane-spanning domain. These results establish that neurons have the capacity to synthesize MMP-9, which, on activation, may degrade extracellular substrates such as beta-amyloid. Because the latent form of MMP-9 accumulates in AD brain, it is hypothesized that the lack of enzyme activation contributes to the accumulation of insoluble beta-amyloid peptides in plaques.
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PMID:Matrix metalloproteinase-9 (MMP-9) is synthesized in neurons of the human hippocampus and is capable of degrading the amyloid-beta peptide (1-40). 898 19

The molecular nature of lead-induced mutations was examined in this study to more thoroughly understand lead mutagenesis. Chinese hamster ovary K1 cells were exposed to 0.5-3 mM lead acetate for 24 h. The median lethal dose (LD50) value was 1.5 mM, and the hypoxanthine guanine phosphoribosyltransferase (HPRT) mutant frequency increased linearly as lead concentrations were raised from 0.5 to 1.5 mM. We also amplified the HPRT cDNAs of 56 independent lead-induced mutants by reverse transcriptase-polymerase chain reaction (PCR). Forty-two mutant cDNAs were successfully amplified: 36 mutants had transcripts of normal or slightly smaller than normal size, and six mutants had large deletions. The other 14 mutants whose HPRT cDNA could not be amplified were subjected to genomic-DNA PCR analysis. All of those mutants had one or more exons missing from their genomic HPRT DNA. DNA sequencing of mutant cDNAs showed that 22 had single-base substitutions, four had small alterations, 10 had single-exon deletions, and six were missing two or three exons. Furthermore, DNA sequencing of the HPRT intron-exon boundaries in eight splice mutants revealed that all of them had single-base substitutions in their genomic DNA. G.C base substitutions occurred 3.3-fold more frequently than A.T base substitutions. Similar frequencies were observed for G.C-->A.T, G.C-->T.A, and G.C-->C.G mutations. These results suggest that G.C base pairs may be the primary target sites for lead mutagenesis.
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PMID:Lead acetate mutagenicity and mutational spectrum in the hypoxanthine guanine phosphoribosyltransferase gene of Chinese hamster ovary K1 cells. 898 11

Upon prolonged treatment with various antiretroviral nucleoside analogs such as 3'-azido-3'-deoxythymidine, 2',3'-dideoxyinosine, 2',3'-dideoxycytidine, (-)- beta-L-2', 3'dideoxy-3'thiacytidine and 2',3'-didehydro-3'-deoxythymidine, selection of human immunodeficiency virus type 1 (HIV-1) strains with mutations in the reverse transcriptase (RT) gene has been reported. We designed a reverse hybridization line probe assay (LiPA) for the rapid and simultaneous characterization of the following variations in the RT gene: M41 or L41; T69, N69, A69, or D69; K70 or R70; L74 or V74; V75 or T75; M184, I184, or V184; T215, Y215, or F215; and K219, Q219, or E219. Nucleotide polymorphisms for codon L41 (TTG or CTG), T69 (ACT or ACA), V75 (GTA or GTG), T215 (ACC or ACT), and Y215 (TAC or TAT) could be detected. In addition to the codons mentioned above, several third-letter polymorphisms in the direct vicinity of the target codons (E40, E42, K43, K73, D76, Q182, Y183, D185, G213, F214, and L214) were found, and specific probes were selected. In total, 48 probes were designed and applied to the LiPA test strips and optimized with a well-characterized and representative reference panel. Plasma samples from 358 HIV-infected patients were analyzed with all 48 probes. The amino acid profiles could be deduced by LiPA hybridization in an average of 92.7% of the samples for each individual codon. When combined with changes in viral load and CD4+ T-cell count, this LiPA approach proved to be useful in studying genetic resistance in follow-up samples from antiretroviral agent-treated HIV-1-infected individuals.
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PMID:Line probe assay for rapid detection of drug-selected mutations in the human immunodeficiency virus type 1 reverse transcriptase gene. 902 Nov 81


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