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:3.1.27.1 (RNase)
16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antitumor activity of a marine bacterium, Vibrio anguillarum, against Ehrlich carcinoma cells in ddY mice was investigated. The aqueous layer obtained by the hot phenol-water procedure exhibited more antitumor activity than did the middle layer or the phenol layer. This finding indicates that lipopolysaccharide (LPS) derived from V. anguillarum exhibits significant antitumor activity. In fact, mice injected with LPS obtained by ultracentrifugation and treatment with RNase had a longer mean survival period than the control mice. V. anguillarum LPS also inhibited the growth of syngeneic fibrosarcoma induced by 3-methylcholanthrene in C57BL/6 mice. V. anguillarum LPS possesses no 2-keto-3-deoxyoctonate, a regular sugar component of the core region of most gram-negative bacterial LPS, suggesting that 2-keto-3-deoxyoctonate is unnecessary for the antitumor activity of LPS.
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PMID:Antitumor activity of 2-keto-3-deoxyoctonate-free lipopolysaccharide of Vibrio anguillarum in mice. 686 49

Lipid A induced bone marrow cells derived from lipopolysaccharide responder strain C3H/HeN to release a component to the extracellular fluid that enhanced DNA synthesis of splenocytes derived from the lipopolysaccharide nonresponder strain C3H/HeJ. The mitogenic component was not selected when C3H/HeN splenocytes were used instead of bone marrow. The target cell in splenocyte populations responding to the mitogenic component released by lipid A-stimulated bone marrow cells is a B cell, as judged by the corresponding of individual cells undergoing DNA synthesis determined by autoradiograph and the presence of surface immunoglobulin detected by immunofluorescence. The mitogenic factor is heat-labile, sensitive to trypsin, and intensive to RNase.
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PMID:A novel mitogen released by lipid A-stimulated bone marrow cells. 697 87

Hemolin is an insect protein which belongs to the immunoglobulin superfamily and is strongly induced upon bacterial infection. It has been isolated from two moths, Hyalophora cecropia and Manduca sexta. We have isolated and sequenced a genomic clone for hemolin in H. cecropia, in order to resolve its organization and as a basis for investigating hemolin gene regulation. According to Southern-blot analysis, hemolin is encoded by a single gene, Hemolin. It contains six exons ranging over 32-603 bp. The introns are positioned both within and between the immunoglobulin-like domains, a feature typical for cell-adhesion molecules belonging to the immunoglobulin superfamily. By an RNase protection assay, we show that the Hemolin transcript is strongly induced not only by bacteria, but also by lipopolysaccharide and phorbol 12-myristate 13-acetate. Analysis of the upstream region and introns revealed potential binding sites for the Cecropia immunoresponsive factor (CIF), which recognizes the kappa B-like consensus GGGRA YYYYY.
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PMID:Structure and expression of Hemolin, an insect member of the immunoglobulin gene superfamily. 760 Nov 54

Spontaneous production of insulin-like growth factor-I (IGF-I) by inflammatory macrophages contributes to aberrant wound healing, but little is known about regulation of IGF-I synthesis in myeloid cells. The T cell-derived cytokine interferon-gamma (IFN gamma) inhibits several fibrogenic and angiogenic components of the wound-healing response. We have used metabolic labeling of primary colony stimulating factor-1 (CSF-1)-derived macrophages and a transformed macrophage cell line (PU5-1R) followed by immunoprecipitation to demonstrate that synthesis of the 17 kilodalton (kDa) prepro-IGF-I protein by these cells is substantially inhibited by IFN gamma. An exon 4 IGF-I/beta-actin riboprobe expression cassette was used in RNase protection assays to show that IFN gamma also reduces steady state levels of IGF-I mRNA in three different populations of macrophages in a time- and dose-dependent manner. This effect is specific for IFN gamma because neither the IFNs-alpha/beta nor lipopolysaccharide (LPS) affects expression of steady state IGF-I transcripts. Down-regulation of IGF-I mRNA by IFN gamma is dependent on de novo protein synthesis and is abrogated by coculture with cycloheximide. Nuclear run-on assays revealed that elongation of IGF-I transcripts is absent in fresh bone marrow cells but is induced several-fold after cells are cultured for 6 days with CSF-1. Treatment of these CSF-1-derived macrophages with IFN gamma for 6 h substantially inhibits synthesis of IGF-I mRNA. Studies on the decay of IGF-I mRNA in PU5-1R macrophages treated with an RNA polymerase inhibitor confirmed that the decline in IGF-I steady state mRNA in IFN gamma-treated cultures arises from an inhibition of transcription rather than from a reduction in mRNA stability. Since a variety of inflammatory mediators can induce expression of IGF-I in macrophages, inhibition of macrophage IGF-I synthesis by IFN gamma provides a mechanism by which leukocytes regulate levels of this growth factor in their microenvironment.
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PMID:Interferon-gamma inhibits macrophage insulin-like growth factor-I synthesis at the transcriptional level. 777 81

Treatment of Pseudomonas aeruginosa with metal ion chelators, especially ethylenediaminetetraacetic acid (EDTA), causes both release of protein-lipopolysaccharide complexes and cell death. We have examined the effect of EDTA on P. aeruginosa and found that EDTA does not induce the rapid solubilization of the peptidoglycan sacculus and complete lysis as previously thought; the decrease in optical density of cultures incubated with EDTA is primarily due to the loss of the outer membrane. Of the other potential solubilizers examined, only ethylene-bis(oxyethylenenitrilo)tetraacetic acid (EGTA) resulted in some decrease in optical density. The lytic effect of EDTA on 12 strains of P. aeruginosa was examined and was found to vary greatly between strains; the sensitivity to EDTA varies from between 96% and 10% of the decrease in optical density resulting from incubation of cells with both EDTA and lysozyme. Sensitivity to EDTA is not constant during the growth of P. aeruginosa; in the early exponential phase of growth, cells treated with EDTA exhibit a 82% decrease in optical density after 30 min while in the stationary phase the optical density decreases by only 40%. Nucleic acids were observed to leak from cells following treatment with EDTA and this was greatly facilitated by DNase and RNase. The release of genetic material was much reduced when cells were incubated at 4 degrees C, supporting an enzymatic role in cell wall solubilization. We propose that only small areas of the sacculus become hydrolysed via specific peptidoglycan hydrolases, or autolysin(s), which are activated or de-regulated by EDTA.
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PMID:Role of autolysins in the EDTA-induced lysis of Pseudomonas aeruginosa. 800 62

The expression of neurotrophin and neurotrophin receptor mRNAs was examined using RNase protection assays and Northern-blot analysis in rat thymus, spleen tissue and immunocompetent mononuclear cells purified from these two organs. Nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4 mRNAs were all expressed in thymus and spleen tissue although at different levels, while immunocompetent cells expressed neurotrophin-3 and neurotrophin-4 mRNAs. Thymus and spleen tissue expressed mRNAs encoding the low-affinity nerve-growth-factor receptor, the non-neuronal TrkA I receptor, the truncated (kinase deficient) and full-length TrkB, and the TrkC receptor. Low-affinity nerve-growth-factor receptor and non-neuronal TrkA I mRNAs were detected in both thymus and spleen immunocompetent cells. In addition, thymus cells expressed neuronal TrkA II mRNA and spleen cells expressed truncated TrkB mRNA. The expression of TrkA I and TrkA II mRNAs was enhanced in both thymus and spleen cells after cell culture. Enhanced levels of neurotrophin-4 mRNA were observed in spleen immunocompetent cells after adrenalectomy. Moreover, the expression of neurotrophin-4 mRNA was up-regulated after stimulation of immune cells with the mitogens concanavalin A or lipopolysaccharide or with the inflammatory mediator leukotriene B4. This suggests that neurotrophin-4 could be secreted by immunocompetent cells and may be involved in inflammatory processes.
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PMID:Expression of mRNA encoding neurotrophins and neurotrophin receptors in rat thymus, spleen tissue and immunocompetent cells. Regulation of neurotrophin-4 mRNA expression by mitogens and leukotriene B4. 805 49

The murine cDNA, encoding the purine catabolic enzyme, ecto-5'-nucleotidase (NT), was cloned and the tissue-specific distribution of both the mRNA and enzyme activity was examined. Starting with kidney RNA and primers based on the known rat sequence, reverse transcriptase-polymerase chain reaction (RT-PCR) was utilized to obtain the complete sequence for the translated portion of the murine cDNA. Murine NT is 94% identical to human NT at the amino acid (aa) level and 86% identical at the nucleotide (nt) level. NT enzyme assays revealed greater than tenfold more NT activity in mature vs. immature murine T- and B-lymphocytes. A similar increase in NT activity was also found when the pre-B-cell line, 70Z/3, was induced to produce surface kappa light chains with lipopolysaccharide (LPS) and gamma-interferon (gamma-IFN). Thus, culture systems in which murine lymphocytes mature may be useful for examining the mechanisms of NT gene regulation, as well as the function of NT in the immune system. In tissues, enzyme activity varied over 30-fold, from the lowest levels in skeletal muscle, thymus and spleen to highest in placenta, kidney and forestomach. Levels of mRNA, as determined by RNase protection assay, showed increased NT expression in the early gestation site, as compared to non-pregnant uterus, and in day-19.5 placenta, as compared to day-13 chorioallantoic placenta. Messenger RNA levels were in general proportional to enzyme activity, except in the lung and glandular stomach where mRNA levels were higher than expected, based on enzyme activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Murine ecto-5'-nucleotidase (CD73): cDNA cloning and tissue distribution. 822 5

The gene encoding the receptor for macrophage colony-stimulating factor 1 (CSF-1), the c-fms protooncogene, is selectively expressed in immature and mature mononuclear phagocytes and trophoblasts. Exon 1 is expressed only in trophoblasts. Isolation and sequencing of genomic DNA flanking exon 2 of the murine c-fms gene revealed a TATA-less promoter with significant homology to human c-fms. Reverse transcriptase primer extension analysis using exon 2 primers identified multiple clustered transcription initiation sites. Their position was confirmed by RNase protection. The same primer extension products were detected in equal abundance from macrophage or nonmacrophage sources of RNA. c-fms mRNA is acutely down-regulated in primary macrophages by CSF-1, bacterial lipopolysaccharide (LPS), and phorbol myristate acetate (PMA). Each of these agents reduced the abundance of c-fms RNA detectable by primer extension using an exon 3 primer without altering the abundance of presumptive short c-fms transcripts detected with exon 2 primers. Primer extension analysis with an intron 2 primer detected products at greater abundance in nonmacrophages. Templates detected with the intronic primer were induced in macrophages by LPS, PMA, and CSF-1, suggesting that each of the agents caused a shift from full-length c-fms mRNA production to production of unspliced, truncated transcripts. The c-fms promoter functioned constitutively in the RAW264 macrophage cell line, the B-cell line MOPC.31C, and several nonhematopoietic cell lines. Macrophage-specific expression and responsiveness to selective repression by LPS and PMA was achieved by the incorporation of intron 2 into the c-fms promoter-reporter construct. The results suggest that expression of the c-fms gene in macrophages is controlled by sequences in intron 2 that act by regulating transcription elongation.
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PMID:Expression of mRNA encoding the macrophage colony-stimulating factor receptor (c-fms) is controlled by a constitutive promoter and tissue-specific transcription elongation. 849 48

It is well established that exogenous RNA is incorporated into eukaryotic cells and is able to exert various biological responses. Little, however, is known about the effects of such RNA on macrophages. In this study, we demonstrate that RNA extracted from macrophages stimulated with Escherichia coli lipopolysaccharide (LPS), referred to as L-RNA, in contrast to RNA from non-stimulated macrophages (N-RNA), induces the release of a macrophage-derived neutrophil chemotactic factor (MNCF) and interleukin-8 (IL-8) from macrophage monolayers. The effect of L-RNA was dependent of the integrity of the polynucleotide chain and was not due to LPS contamination since its ability to induce MNCF and IL-8 release was strongly reduced by RNase but was not affected by DNase or polymyxin B. The poly A(+)L-RNA and poly A(-)L-RNA fractions were able to induce the release of MNCF and IL-8, indicating that the L-RNA could be acting at transcriptional and translational levels. The demonstration that actinomycin-D and cycloheximide inhibited the release of MNCF and IL-8 by L-RNA-stimulated macrophages confirms this assumption. Fractionation of the total L-RNA by centrifugation on a 5-20% sucrose gradient showed that the L-RNA which sediments in the 4-5S region of the gradient is the only fraction capable of inducing the release of MNCF from naive macrophages. We have previously shown that macrophage monolayers stimulated with interleukin-1 beta or LPS release a low molecular RNA which also sediments in the same 4-5S region. Taken together, these results support our proposal that resident macrophages, when activated by injurious stimuli, in addition to secreting cytokines, also release a low molecular weight (4-5S) RNA which may act on the surrounding macrophages to further stimulate the release of cytokines. This process would amplify the inflammatory response and would increase the mechanisms involved in the defense response or tissue injury.
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PMID:Partial characterization of the RNA from LPS-stimulated macrophages that induces the release of chemotactic cytokines by resident macrophages. 859 14

Transcription factor NF-kappaB is essential for the induction of nitric oxide synthase (NOS) II (iNOS) by bacterial lipopolysaccharide in murine macrophages (Xie, Q. W., Kashiwabara, Y., and Nathan, C. (1994) J. Biol. Chem. 269, 4705-4708). In 3T3 fibroblasts, agents other than cytokines are efficacious inducers of NOS II expression. In addition to cytokines such as interferon-gamma or tumor necrosis factor-alpha, protein kinase C-stimulating agents such as tetradecanoylphorbol-13-acetate, or cyclic AMP-elevating agents such as forskolin and 8-bromo-cAMP markedly increased NOS II mRNA (measured by Sl nuclease and RNase protection analyses), NOS II protein (determined by Western blotting), and NOS activity (measured by chemiluminescence detection of NO2-). Transforming growth factor-beta1 (which is an inhibitor of NOS II induction in other cell types) potentiated NOS II mRNA expression produced by all inducing agents listed, whereas dexamethasone, pyrrolidine dithiocarbamate and 3,4-dichloroisocoumarin (inhibitors of NF-kappaB activation) suppressed NOS II mRNA induction in response to all stimulants. In electrophoretic mobility shift assays, nuclear protein extracts from 3T3 cells stimulated with any of the inducing agents significantly slowed the migration of an NF-kappaB-binding oligonucleotide, whereas nuclear extracts from untreated control cells did not. These experiments indicate that NF-kappaB is the key control element for the induction of NOS II in response to at least three different second messenger pathways in 3T3 cells.
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PMID:In murine 3T3 fibroblasts, different second messenger pathways resulting in the induction of NO synthase II (iNOS) converge in the activation of transcription factor NF-kappaB. 862 88


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