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)

Fifty sera containing antinucleolar antibodies were o gathered in a routine laboratory during testing for antinuclear antibodies with indirect immun-fluorescence over a five-year period. The patients involved were suffering from sclerodermia (13 cases), rheumatoid arthritis (7 cases), polymyositis (3 cases), lupus (2 cases), various rhumatismal disease (59 cases) and non rhumatismal diseases in 16 cases, including 5 malignant diseases. In 80 per cent of the cases nucleolar fluorescence was combined with nuclear fluorescence of another type. The antibodies were almost always of the IgG category and belonged in 2/3 of cases to several immunoglobulin categories, most often IgG-IgA. Pretreatment of the liver cuttings with RNase always modifies the nucleolar fluorescence, most often making it negative, and pretreatment with DNase using a combination of enzymes 10 times higher also modifies it (more often decreasing it than making it negative), which indicates that the nucleolar antigen, probably an ARN with a low molecular weight, also depends upon the ADN.
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PMID:[Antinuclear antibodies: immunological characteristics and clinical significance]. 31 10

The interaction of lactoperoxidase with lysozyme and ribonuclease as well as immunoglobulins from cow milk has been investigated. As gel filtration and enzyme kinetics experiments have shown, the lactoperoxidase was slightly activated by complexing to lysozyme, while IgA and IgM were inhibitory for the peroxidase. Oh the other hand, IgG and ribonuclease had no effect on the enzyme activity although the latter did form a complex with the lactoperoxidase. The interaction between the lysozyme and lactoperoxidase appears to be rather specific since the alteration of the lactoperoxidase sugar moiety by periodate oxidation, prevented the formation of the lactoperoxidase-lysozyme complex.
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PMID:Interaction of lactoperoxidase with enzymes and immunoglobulins in bovine milk. 263 59

Human seminal fluid, at low dilutions, prevented the binding of aggregated human IgG (AHG) to bull spermatozoa. Seminal fluids from vasectomized men were also inhibitory. Preincubation of the seminal fluid with the spermatozoa prior to washing and addition to AHG had no inhibitory effect, indicating that the fluid component was reacting directly with AHG. Human seminal fluid was fractionated by gel exclusion chromatography on Ultrogel AcA-34, and AHG inhibitory activity was found in fractions corresponding to a molecular weight of 94,000. The activity in this fraction was stable to boiling for 10 min. It was sensitive to pronase but resistant to glycosidase, phospholipase C, neuraminidase, ribonuclease, and deoxyribonuclease, indicating that it was a protein. The gel filtration fraction readily bound recrystallized Fc and AHG; IgG was bound to a lesser extent, and no reactivity was observed with F(ab')2, IgA, or IgM. Thus, the seminal fluid fraction appeared to specifically react with the Fc portion of IgG. The seminal fluid Fc-binding protein was isolated by affinity chromatography on Fc coupled to CNBr-activated Sepharose 4B. Scatchard analysis revealed that the binding of the seminal fluid Fc-binding protein to recrystallized Fc is reversible and had a Kd of approximately 3 x 10(-6) M.
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PMID:An IgG-Fc binding protein in seminal fluid. 622 60

Antinucleolar antibody (ANoAb) was tested for in sera from 25 patients with systemic lupus erythematosus (SLE), 61 with progressive systemic sclerosis (PSS), 22 with chronic active hepatitis (CAH) and 28 healthy persons, using immunofluorescence reactivity with acetone-fixed monolayers of cultured human fibroblasts, and a procedure to reveal ANoAb when other antinuclear antibodies were concurrently present. ANoAb was found on direct testing in sera from 6 patients with SLE, 15 with PSS and 7 with CAH, but not in any of 28 sera from healthy persons; homogeneously reactive antinuclear antibody was also present in the serum of these 6 cases of SLE, in 6 of the 15 with PSS and in 3 of the 7 with CAH and, in SLE specifically, pre-treatment of fibroblast monolayers with DNase "unmasked" the presence of ANoAb in a further 7 sera which had shown only homogeneous nuclear staining in fibroblasts. ANoAb belonged to the IgG, IgM and IgA class in sera from cases of SLE and PSS, and to only the IgG and IgM class in sera from cases of CAH. ANoAb titres were highest in patients with PSS. ANoAb were sensitive to RNase in 5 cases, to RNase and DNase in 6, and were sensitive to combinations of RNase, DNase, NaC1, and trypsin in the remaining cases. We conclude that (i) fibroblast monolayers are a suitable substrate for the demonstration of ANoAb, (ii) homogeneous staining of cell nuclei may mask ANoAb, so that the incidence of ANoAb becomes higher in SLE than in PSS, (iii) low-titre ANoAb in CAH not visualized in frozen tissue sections may be detected on fibroblast monolayers, and (iv) nucleolar antigens probably include RNA, RNA bound to DNA, and RNA bound to proteins.
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PMID:Antinucleolar autoantibodies demonstrated by monolayers of human fibroblasts in sera from patients with systemic lupus erythematosus, progressive systemic sclerosis and chronic active hepatitis. 674 43

Various polyelectrolytes were investigated regarding their capacity to inhibit the binding of human IgG to Fc-receptors on group A streptococci, type M1. Of cationic substances, protamine and arginine-rich histone inhibited significantly, while lysine-rich histone, concanavalin A, lysozyme, polymyxin B, ribonuclease and tuftsin did not. Of anionic materials, liquoid was inhibitory, in contrast to chondroitin sulphate, dextran sulphate, DNA and heparin. Washing experiments showed that the inhibition was caused by binding of the polyelectrolytes to the streptococci. The finding that heated IgG inhibited the binding of histone to the streptococci also indicated a close relation between the binding sites for these compounds. Diffusion-in-gel experiments with alkaline extract of M1 demonstrated that the substances blocking the IgG Fc-receptor were bound to polyglycerophosphate, suggesting that the inhibition of the IgG uptake was due to interaction with lipoteichoic acid. Leukocyte and platelet extracts could modify the binding of IgG, probably by an enzymatic digestion of the receptors. The arginine-rich histone was also capable of inhibiting the binding of IgG to type M15 group A streptococci and to one group G strain. However, the polyelectrolytes had no effect on the binding of IgG to Staphylococcus aureus or of IgA to type 4 group A streptococci.
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PMID:Cationic polyelectrolytes, liquoid and leukocyte extract modulate the binding of IgG to group A streptococcal Fc-receptors. 704 38

Primary and secondary immunizations with live, attenuated yellow fever virus vaccine (17D strain) were performed in order to study the course of appearance of virus-neutralizing antibodies and immunoglobulin M (IgM) and IgG antibodies directed against the virus and the interferon-dependent enzyme 2',5'-oligoadenylate synthetase (2',5'AS) activity, determined in homogenates of peripheral B and T lymphocytes. From cellular ATP, this enzyme generates 2',5'-oligoadenylates which mediate degradation of viral mRNA by stimulation of a latent RNase. By day 4 after the first immunization, the earliest and highest 2',5'AS activity was present in the T-lymphocyte fraction. By day 7, the enzyme activity was highest in the B-lymphocyte fraction. Virus-neutralizing antibodies appeared on day 7, and IgM antibodies were present on day 12. After the second immunization, performed 2 years +/- 2 months later, the only significant increase in 2',5'AS activity was observed in the T-lymphocyte fraction. Virus-neutralizing antibodies were present from day 1, whereas no IgM antibodies were detected. By day 12, 80% of the vaccines were IgG positive. In the primary and secondary (memory) immune responses, 2',5'AS activity is expressed in the T-lymphocyte fraction prior to the appearance of antibodies directed against the virus and may serve as an early and sensitive marker of an ongoing virus infection which is otherwise difficult to detect. No change in conventional laboratory analysis parameters, such as in differential blood cell counts or total IgA, IgG, and IgM, disclosed the immune activity in either the primary or the secondary immunization.
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PMID:Lymphocytic 2',5'-oligoadenylate synthetase activity increases prior to the appearance of neutralizing antibodies and immunoglobulin M and immunoglobulin G antibodies after primary and secondary immunization with yellow fever vaccine. 766 76

The induction of immunoglobulin E (IgE) switching in B cells requires at least two signals. The first is given by either of the soluble lymphokines interleukin 4 (IL-4) or IL-13, whereas the second is contact dependent. It has been widely reported that a second signal can be provided by the CD40 ligand (CD40L) expressed on the surface of T cells, mast cells, and basophils. A defect in the CD40L has been shown recently to be responsible for the lack of IgE, IgA, and IgG, characteristic of the childhood X-linked immunodeficiency, hyper IgM syndrome (HIGM1). IgE can however be detected in the serum of some HIGM1 patients. In this study, we isolated T cell clones and lines using phytohemagglutinin (PHA) and allergen, respectively, from the peripheral blood of one such patient who expressed a truncated form of CD40L, and investigated their ability to induce IgE switching in highly purified, normal tonsillar B cells in vitro. Unexpectedly, 4 of 12 PHA clones tested induced contact-dependent IgE synthesis in the presence of exogenous IL-4. These clones were also shown to strongly upregulated IL-4-induced germline epsilon RNA and formed dense aggregates with B cells. Of the four helper clones, three were CD8+, of which two were characteristic of the T helper cell 2 (Th2) subtype. Two allergen-specific HIGM1 T cell lines, both of the Th0 subtype, could also drive IgE synthesis when prestimulated using specific allergen. All clones and lines were negative for surface expression of CD40L, and the mutated form of CD40L was confirmed for a representative clone by RNase protection assay and sequencing. The IgE helper activity could not be attributed to membrane tumor necrosis factor alpha (TNF-alpha) although it was strongly expressed on activated clones, and the addition of neutralizing anti-TNF-alpha antibody did not abrogate IgE synthesis. These results therefore suggest the involvement of T cell surface molecules other than CD40L in the induction of IgE synthesis, and that these molecules may also be implicated in other aspects of T-B cell interactions.
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PMID:T cell clones from an X-linked hyper-immunoglobulin (IgM) patient induce IgE synthesis in vitro despite expression of nonfunctional CD40 ligand. 796 60

Transport of secretory IgA into external fluids is mediated by the polymeric immunoglobulin receptor (pIgR) on the surface of mucosal epithelial cells. We studied the mechanism by which interferon-gamma (IFN-gamma) induces pIgR expression in HT-29.74 cells, a subclone of the HT-29 cell line selected for high concns of pIgR. Here we report the isolation of genomic DNA and cDNA clones encoding human pIgR and development of a sensitive ribonuclease protection assay for pIgR mRNA. This assay was used to determine if induction of pIgR by IFN-gamma is mediated by accumulation of pIgR mRNA. After an initial lag of 12 hr, pIgR mRNA increased seven-fold in response to IFN-gamma, reaching a plateau at 24 hr. Concentrations of pIgR protein also increased seven-fold, but the increase was delayed until 48 hr following stimulation with IFN-gamma. Cycloheximide treatment abolished the IFN-gamma induced increase in pIgR mRNA, indicating that induction of pIgR mRNA by IFN-gamma requires de novo protein synthesis. These results suggest that induction of pIgR expression by IFN-gamma involves an increase in steady-state concns of pIgR mRNA via a protein synthesis dependent mechanism.
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PMID:Interferon-gamma induces polymeric immunoglobulin receptor mRNA in human intestinal epithelial cells by a protein synthesis dependent mechanism. 845 39

Molecular cloning techniques have recently demonstrated that rabbit has 13 different IgA C alpha H chain genes. This is in contrast to human and mouse that have only two and one C alpha heavy chain genes, respectively. In previous studies, nucleotide sequence analysis indicated that the 13 rabbit C alpha genes were potentially functional, and in vitro expression experiments showed that at least 12 of these genes were expressible. To understand the role of these multiple IgA isotypes we analyzed RNA of various lymphoid tissues for the presence of mRNA representing each of the multiple C alpha genes. We used the RNase protection assay with probes that are specific for the 13 different C alpha genes and we consistently found that at least 10 of the C alpha genes are expressed, albeit at different levels, in gut (small intestines), appendix, mesenteric lymph node, and mammary tissue. However, in salivary gland (submandibular), only seven of these genes are expressed at significant levels and in lung and tonsil only one C alpha gene, C alpha 4, is expressed at a level comparable to its expression in other tissues. Analysis of RNA of Peyer's patch showed differences in the level of C alpha gene expression between different animals and between different Peyer's patches of the same rabbit; in some cases, most of the C alpha genes were expressed, but in some cases only C alpha 4 was expressed at a significant level. Inasmuch as C alpha 4 is the 5' most C alpha gene we propose that IgA-producing cells are derived from B cells that have initially undergone isotype switching to C alpha 4 and we discuss various mechanisms that could explain switching to the more 3' C alpha genes.
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PMID:Differential expression of 13 IgA-heavy chain genes in rabbit lymphoid tissues. 851 70

Receptors for the Fc portion of IgA (Fc alpha R) trigger important immunological elimination processes against IgA-coated targets. Investigation of human Fc alpha R (CD89) transcripts in neutrophils, eosinophils and a monocyte-like cell line, THP-1, with the use of reverse transcriptase PCR, Northern blotting and RNase protection analysis, has provided evidence in these cell types for at least two distinct transcripts generated by alternative splicing. The cDNAs derived from the two major transcripts of both neutrophils and eosinophils have been cloned and sequenced. For both cell types, the larger clone represents the previously described full-length receptor, whereas the second, shorter, splice variant lacks the entire second, membrane-proximal, Ig-like domain. Stable CHO-K1 transfectants have been obtained for both full-length and truncated variant neutrophil receptors. Whereas the full-length receptor is recognized by a panel of five anti-Fc alpha R monoclonal antibodies (mAbs), the shorter variant is bound weakly by only two of the antibodies, suggesting that the epitopes recognized by the majority of the mAbs lie at least in part in the second Ig-like domain of Fc alpha R. Both full-length and splice variant forms of the receptor bind secretory IgA, but the weak binding to serum IgA seen with the full-length receptor is not evident with the shorter variant. Alternative splicing might therefore serve as a means of diversifying Fc alpha R structure and function.
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PMID:Alternative splicing of the human IgA Fc receptor CD89 in neutrophils and eosinophils. 883 18


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