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 strain-dependent expression of murine serum amyloid P-component (SAP) has been known to be linked to the Sap locus. We have quantified the SAP mRNA in several inbred strains including DBA/2 and C57BL/6 mice which represent high and low producers of SAP at resting state, respectively, and found that the mRNA levels correlated well with the amount of SAP protein. Interestingly, the SAP mRNA level of F1 mouse between DBA/2 and C57BL/6 was low and similar to that of C57BL/6. Primer extension and ribonuclease (RNAase) protection analyses demonstrated that a single type of transcript was generated from the SAP gene and that the cap sites were identical regardless mouse strains tested under unstimulated and stimulated (by lipopolysaccharide (LPS) or interleukin-6 (IL-6)) conditions. To investigate possible structural difference of the SAP gene including 5' flanking region, we have cloned, sequenced and compared the SAP genes from DBA/2 and C57BL/6 mice. Sequence analyses revealed that the 5' flanking regulatory regions, as well as the coding regions, were well-conserved between the two strains. These results demonstrate that the strain-dependent SAP expression occurs at the transcriptional level but seems to be affected by neither different type of the transcripts nor structural difference of the 5' flanking and coding regions of the SAP gene. It was suggested that a possible transcription factor with suppressive activity, which is encoded by a gene linked to Sap, may be involved.
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PMID:The strain-dependent constitutive expression of murine serum amyloid-P component is regulated at the transcriptional level. 162 42

Overlapping murine genomic DNA fragments containing the entire cDNA sequence were isolated from a cosmid library prepared from the DBA/2J strain of mice. The gene is more than 80-kb long, consisting of 16 exons. All of the exon-intron boundaries have been defined. The organization of the gene is highly conserved between the murine and human genes at least for the several exons and introns for which information for the human gene is available [Morreau et al., J. Biol. Chem. 264:20655, 1989]. Primer extension and RNase protection experiments indicated the presence of three potential transcription initiation sites, which are preceded by GC-rich SP1 binding sites but without typical TATA or CAT boxes, as is often the case for genes coding for housekeeping proteins. Compared to the cDNA sequence from C57BL/6J mouse, there were five nucleotide polymorphisms in the protein-coding region, two of which resulted in altered amino acids.
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PMID:Organization of the mouse acid beta-galactosidase gene. 190 71

The 43-kDa non-O antigenic component isolated from the crude ribosomal fraction of Salmonella typhimurium [9] was further purified by affinity chromatography (43-kDa protein: 43-kDp). Immunization with 43-kDp did not induce complete mouse protection in CF1 mice to 500 LD50 of S. typhimurium, although it elicited a substantial IgG antibody response. The 43-kDp exhibited the mitogenicity to splenocytes (CF1 and C3H/HeJ) and B cell-rich populations (CF1). Complexing 43-kDp with the compact ribosomes of Streptococcus pyogenes by formaldehyde (complex vaccine: CV) elicited both IgM and IgG antibodies to 43-kDp. CV induced a boosting effect to enhance IgG antibody response. Moreover, CV generated delayed-type hypersensitivity to salmonella antigens and also conferred complete protection against 500 LD50 challenge of S. typhimurium to CF1 mice. These abilities of CV were reduced or impaired by RNase digestion. CV was able to induce partial or complete protection in inbred mouse strains (C3H/HeN, C3H/HeJ, DBA/2 and A/J). These data, in addition to other reports, suggest that conformational stability between ribosomes and contaminating substances such as 43-kDp or O-antigens might be required for the overall effects of the ribosomal vaccine.
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PMID:Requirement of the conformational stability of a Salmonella ribosomal vaccine for its mouse protection. 193 Nov 35

Multidrug-resistance (MDR) genes are induced in the liver of rodents treated with a variety of foreign chemicals and hepatocarcinogens. It has been reported that 2,3,6,7-tetrachlorodibenzo-p-dioxin (TCDD) might increase hepatic MDR transcripts in the Fischer rat and the C57BL/6 (B6) inbred mouse strain having the high-affinity aromatic hydrocarbon (Ah) receptor, but not in the DBA/2 (D2) strain having the low-affinity Ah receptor. These intriguing results suggest that TCDD might activate MDR gene expression by way of an Ah receptor-mediated signal transduction pathway. We have attempted to confirm these data in four inbred mouse strains: two (B6 and BALB/c) having the high-affinity Ah receptor, and two (D2 and AKR) having the low-affinity Ah receptor. The RNase protection assay was used to distinguish between the MDR1, MDR2, and MDR3 mRNAs. TCDD treatment at high (100 micrograms/kg) and low (1 mu/kg) doses, a time course from 6 to 96 hr of TCDD treatment, progeny from the B6D2F1 x D2 backcross, and transcriptional run-on experiments were performed. The Cyp1a-1 (cytochrome P1450) and Nmo-1 [NAD(P)H:menadione oxidoreductase] genes, two members of the TCDD-inducible [Ah] battery, were used as positive controls. We were unable to detect significant coinduction of MDR1, MDR2, or MDR3 mRNA with CYP1A1 mRNA or with Cyp1a-1 or Nmo-1 transcription under any conditions. Therefore, we conclude that any effects that TCDD might have on MDR expression must be substantially different from TCDD effects on genes known to be induced via the Ah receptor.
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PMID:Murine mdr-1, mdr-2, and mdr-3 gene expression: no coinduction with the Cyp1a-1 and Nmo-1 genes in liver by 2,3,7,8-tetrachlorodibenzo-p-dioxin. 206 18

The ability of polyribosomes, obtained from several bacterial species, to suppress the development of cutaneous SaD2 fibrosarcomas in DBA/2 mice were evaluated. Suppression of tumor appearance depended upon the tumor load at the time of treatment, dose of polyribosomes, and species source of polyribosomes, with Serratia marcescens being superior to Escherichia coli, Streptococcus pneumoniae, Mycobacterium bovis (Pasteur), Mycobacterium smegmatis, and Propionibacterium acnes (formerly Corynebacterium parvum). A single injection of 5 or 50 microgram of Serratia polyribosomes at the tumor site 72 hr after the intradermal administration of 1.5 X 10(3) SaD2 cells resulted in 66 to 95% survival. All untreated animals expired within 50 days. Tumor suppression occurred at both flank and footpad sites. Presensitization with polyribosomes and incorporation of polyribosomes into adjuvant were not required for the tumor-suppressive effect. Treatment of Serratia polyribosomes with RNase or pronase reduced the number of survivors. Endotoxin was not detectable with the Limulus amebocyte lysate assay.
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PMID:Tumor-immunotherapeutic efficacy of Serratia marcescens polyribosomes. 615 30

P-815 mastocytoma cells from DBA/2 mice and a 3-methylcholanthrene-induced fibrosarcoma from C57BL/6 mice produced in culture at least two soluble anti-inflammatory factors that inhibited macrophage accumulation in vivo when the factors were injected sc into syngeneic recipients. One factor was a low-molecular-weight peptide (less than 1,000), as judged by ultrafiltration, failure of extraction by lipid solvents, nonsusceptibility to DNase or RNase, partial inactivation by trypsin, and complete inactivation by carboxypeptidase B. The second anti-inflammatory factor had a molecular weight between 30,000 and 100,000 and was also not extractable with lipid solvents. Production of anti-inflammatory factors by P-815 mastocytoma cells was inhibited by cycloheximide and cell irradiation but not by colchicine pretreatment of the cells, suggesting a relationship to protein synthesis rather than cell growth. Soluble anti-inflammatory factors depressed granulocyte as well as macrophage responses. Anti-inflammatory factors were not found in supernatants from cultures of splenocytes, peritoneal exudate cells, or murine lung fibroblasts.
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PMID:Characterization of anti-inflammatory factors produced by murine tumor cells in culture. 681 63

An elevated expression of TNF-alpha in embryonic microenvironment was found to be associated with postimplantation loss. In this work, we examined the pattern of TNF-alpha expression at both the mRNA and the protein level as well as the distribution of TNF-alpha receptor mRNA in the uteroplacental unit of mice with induced (cyclophosphamide-treated) or spontaneous (CBA/J x DBA/2J mouse combination) pregnancy loss. RNase protection analysis demonstrated an increase in TNF-alpha mRNA expression in the placentae of mice with pregnancy loss compared with that in control mice. TNF-alpha messages were localized to the uterine epithelium and stroma as well as the giant and spongiotrophoblast cells of the placenta. The intensity of the hybridization signal in placentae of mice with pregnancy loss was substantially higher than that in control mice. The up-regulation of TNF-alpha mRNA was accompanied by an increase in the expression of TNF-alpha receptor I mRNA in the same cell populations. The elevation of TNF-alpha production was also demonstrated at the protein level. Western blot analysis showed an increased level of the 18- and 26-kDa TNF-alpha protein species in the uteroplacental unit of mice with pregnancy loss. Immunostaining revealed TNF-alpha-positive leukocytes located in the uterus and placenta. Finally, we found that immunization of mice with cyclophosphamide-induced pregnancy loss while decreasing the resorption rate in these females resulted in a decline in TNF-alpha expression at the fetomaternal interface. These data clearly suggest an involvement of TNF-alpha in pathways leading to both spontaneous and induced placental death.
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PMID:TNF-alpha messenger RNA and protein expression in the uteroplacental unit of mice with pregnancy loss. 957 30

CSF-1 plays an important role in female reproduction and normal embryo development. To understand further CSF-1 function in normal and, especially, in compromised pregnancy, we studied the pattern of its mRNA expression as well as expression of its receptor (c-fms) in the uteroplacental units of mice with induced (cyclophosphamide (CY)-treated) and spontaneous (CBA/J x DBA/2J mating combination) pregnancy loss. RNase protection analysis demonstrated the presence of two forms of CSF-1 mRNA in the uteroplacental unit corresponding to 1400- and 263-bp protective fragments. Densitometric analysis demonstrated that the level of 1400-bp mRNA form was decreased by 40% in the uteroplacental units of mice with CY-induced pregnancy loss compared with the control mice. About 20% decrease in 263-bp protective fragment was registered in resorbing versus non-resorbed placenta of CBA/J females mated to DBA/2J males. As judged by in situ hybridization assay, CSF-1 mRNA transcripts were localized in the uterine epithelium and stroma, while c-fms mRNA was found mainly in the trophoblast. The number of metrial gland cells as well as the number of uterine leucocytes expressing CSF-1 and c-fms mRNAs was substantially lower in the uteroplacental unit of mice with pregnancy loss than in control animals. Maternal immunostimulation, while significantly decreasing the resorption rate in mice with CY-induced pregnancy loss, also strengthened CSF-1 mRNA expression at the fetomaternal interface and resulted in reconstitution in the number of CSF-1+ uterine leucocytes and metrial gland cells. These data suggest a role for uterine CSF-1 in the physiology of normal and compromised pregnancy and demonstrate a possible involvement of CSF-1-associated signalling in mechanisms of placenta and endometrium repair following immunopotentiation.
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PMID:Colony-stimulating factor-1 (CSF-1) expression in the uteroplacental unit of mice with spontaneous and induced pregnancy loss. 1046 60

Chronic ethanol treatment is known to alter gene expression and function of gamma-aminobutyric acid type-A (GABA(A)) receptors. Here we focus on the beta(2) subunit which is widely expressed in the mammalian brain, and plays a key role in the GABA binding site. Previous studies using rodent models of ethanol dependence show either increased or no change of beta(2) subunit mRNA and peptide content following chronic ethanol administration. In humans, polymorphism at the beta(2) subunit is associated with ethanol dependence in some, but not all, populations. In the present study we measured mRNA content in the cerebellum and cerebral cortex using ethanol-naive and ethanol-dependent DBA/2J and C57BL/6J mice. The DBA/2J strain displays severe ethanol withdrawal severity, while the C57BL/6J strain shows milder withdrawal reactions. RNase protection analysis demonstrated that the DBA/2J strain is more sensitive to ethanol-induced increases in beta(2) subunit mRNA content in the cerebellum, showing significant increases at lower blood ethanol concentrations than C57BL/6J mice. The ethanol-induced regulation in C57BL/6J mice appears to be more complex, with decreases in beta(2) subunit mRNA content at low blood ethanol concentrations, and increases at higher concentrations. These data suggest that differences between C57BL/6J and DBA/2J mice in the degree of physical dependence (withdrawal) on ethanol may be related to differential sensitivity to ethanol regulation of beta(2) subunit expression.
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PMID:GABA(A) receptor beta(2) subunit mRNA content is differentially regulated in ethanol-dependent DBA/2J and C57BL/6J mice. 1087 96