Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.5 (RNase)
 17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunosuppressor T cells (IST),6 capable of inhibiting the rejection of a methylcholanthrene-induced fibrosarcoma (S1509a) in A/Jax mice immune to this tumor, produced soluble factors with similar suppressive activity. The immunosuppressive factor(s) (ISF) has been shown to be immunologically specific, as demonstrated by the complete loss of suppressive activity after absorption with S1509a cells, but not with cells of an unrelated syngeneic tumor. From its behavior on gel filtration, the size of ISF was deduced to be less than 70,000 daltons. The ISF was not removed by passage through a rabbit anti-mouse F(ab')2 reverse immunosorbent and, hence, it was concluded that ISF was not likely to be an immunoglobulin. The (immunosuppressive) activity of ISF was destroyed by treatment with Pronase, but not with RNase. The ISF was found to share the antigenic determinant(s) of the product(s) of the K end of the major histocompatibility complex of the mouse. Moreover, antibodies to ISF were induced by immunization with ISF-tumor cell complexes. Thus, IST and their factor(s) appear to play an important role in the regulation of the immune response to tumor antigens.
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PMID:Regulation of the immune response to tumor antigens. III. Characterization of thymic suppressor factor(s) produced by tumor-bearing hosts. 6 67

In vivo experiments performed with NIH (nu/nu, bg/bg, xid/xid) triple immunodeficient (TD) mice revealed the striking ability of i.v. injected B16-F1 and B16-F10 murine melanoma cells to colonize not only the lungs but also the liver of TD mice. Subsequently, B16 melanoma cell cultures, which express very low levels of H-2Kb antigen, were cotransfected with plasmids pRSVneo, containing the neomycin resistance gene, and 6-2B1pMT, expressing the H-2Kb complentary DNA under the control of the metallothionein enhancer-promoter. Several neomycin-resistant clones were analyzed for H-2Kb and H-2Db expression by RNase protection and flow cytometry assays. All parental lines and transfected clones expressed normal levels of H-2Db mRNA, while only some of the transfected clones expressed easily detectable levels of H-2Kb mRNA. Moreover, in these clones H-2Kb expression could be enhanced in the presence of Zn2+, indicating that the metallothionein enhancer was functioning properly. Parental cells and transfected clones were injected i.v. in TD mice to assess the possible involvement of H-2Kb antigen in regulating the metastatic potential of B16 melanoma cells. We observed a remarkable correlation between expression of H-2Kb antigen and suppression of liver-specific metastases in TD mice. Identical results were obtained when we gave TD mice injections of mixed populations of transfectants expressing H-2Kb antigen, obtained by fluorescence-activated cell sorting. These experiments allowed us to rule out the possibility that the observed changes in metastatic potential were due to clonal variability among individual transfected clones. Taken together, the results of our in vivo studies with immunodeficient mice support the notion that specific major histocompatibility complex Class I molecules modulate the metastatic potential of malignant cells also by mechanisms which are independent of their well-established role in antigen presentation.
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PMID:Expression of a transfected H-2Kb gene in B16 cells correlates with suppression of liver metastases in triple immunodeficient mice. 161 80

The binding of immunogenic peptides to class II major histocompatibility molecules was examined at various pH values. We studied binding of peptides containing residues 52-61 from hen egg lysozyme (HEL) to I-Ak on fixed peritoneal macrophages or to solubilized affinity-purified I-Ak. Optimum binding occurred at pH 5.5-6.0 with accelerated kinetics relative to pH 7.4; equilibrium binding was also higher at pH 5.5-6.0 than at 7.4. Similar enhancement at pH 5-6 was observed for the binding of hemoglobin-(64-76) to I-Ek and of ribonuclease-(41-61) to I-Ak. In contrast, the binding of HEL-(34-45) to I-Ak was minimally enhanced at acid pH. Dissociation of cell-associated or purified peptide-I-Ak complexes was minimal between pH 5.5 and 7.4, with increased dissociation only at or below pH 4.0 [HEL-(46-61)] or pH 5.0 [HEL-(34-45)]. Thus, optimum peptide binding occurs at pH values similar to the endosomal environment, where the complexes appear to be formed during antigen processing. In addition, we examined the effect of a number of polysaccharides on the binding of peptide to I-Ak. None of these competed with the HEL peptide 125I-labeled YE52-61 for binding to I-Ak. [3H]Dextran also failed to bind purified I-Ak. Polysaccharides do not appear to bind to class II major histocompatibility complex molecules, which explains the T-cell independence of polysaccharide antigens.
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PMID:Effects of pH and polysaccharides on peptide binding to class II major histocompatibility complex molecules. 201 83

The retrotransposon micropia was first described from Y-chromosomal fertility genes of Drosophila hydei. Screening a Drosophila melanogaster genomic library yielded several clones representing micropia elements in D. melanogaster. The DNA sequences of two elements from D. hydei (micropia-DhMiF2 and micropia-DhMiF8) and two elements from D. melanogaster (micropia-Dm2 and micropia-Dm11) permitted a detailed analysis of the spatial organization of micropia constituents. Micropia represents the typical gene organization represented by "core"-protein domains followed by a protease, reverse transcriptase, RNase and integrase domain. New features of the micropia family compared with other retrotransposons are: (1) a region of similarity to class I major histocompatibility complex antigens of mammals; (2) only one main open reading frame of about 4000 bases length; (3) a non-protein-coding region of about 500 base-pairs length between the 3' end of the open reading frame and the 5' start of the 3' long terminal repeat. This region includes 32 base-pair tandem repeats; (4) within the long terminal repeats, 82 base-pair tandem repeats with four potential ecdysteroid receptor binding sites. Because micropia combines many evolutionary features of different viruses, non-viral transposable elements, chromosomal genes and repetitive sequence organizations, this retrotransposon may be seen as a "minigenome" reflecting evolutionary principles of the construction of genomic components.
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PMID:Micropia: a retrotransposon of Drosophila combining structural features of DNA viruses, retroviruses and non-viral transposable elements. 246 89

Enhancer-like sequences have previously been identified in the promoter region of the mouse major histocompatibility complex (MHC) class I genes. We have screened for such sequences in and around a human MHC class I gene, HLA-B7. Various restriction fragments of the B7 gene were assayed for their ability to enhance transcription of a bacterial chloramphenicol acetyltransferase gene from a simian virus 40 promoter in transiently transfected mouse LTA cells. Our results demonstrate that enhancer activity is located in introns 3 and 5 as well as 5' to the transcription initiation site. RNase protection experiments corroborate the results. Preliminary experiments indicate that B7 enhancers are active in various cell types. The role of these enhancers in B7 gene expression is not known at present. We speculate that the position of the enhancer elements may be related to the occurrence of Hpa II tiny fragment islands.
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PMID:Multiple enhancer-like sequences in the HLA-B7 gene. 250 82

A unique 2.2-kb mRNA is transcribed from the Q6 and Q8 genes of the mouse major histocompatibility complex. RNase protection experiments and DNA sequence analysis have mapped the 3' terminus to a site located 1110 bp downstream from exon 8. Comparison of the 3' sequence of Q8 to that of Q7 revealed that the two genes diverge from one another at a point located 200 bp into the untranslated domain. This finding explains the increased size of the transcript. RNase protection experiments involving twelve different strains of mice have revealed few sequence polymorphisms. A tissue distribution of the 2.2-kb transcript in B6 mice revealed that the highest quantities of message were present in the spleen with decreasingly lower amounts in the thymus, liver, kidney, testis, and brain. The H-2r haplotype appeared novel; it is phenotypically Qa-2-, yet expressed a 2.2-kb transcript which hybridizes to a Q8 probe. A comparison of a Qa-2hi expressor, B6, and a Qa-2low expressor, BALB/cFla, has established that these quantitative cell surface differences are reflected in mRNA differences. A homology search of the Genbank database has revealed that the 3' portion of Q8 contains extensive homology to a retrovirus-like long terminal repeat sequence that is characteristic of an embryonic-specific transposon (ETn).
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PMID:Genetics and expression of the Q6 and Q8 genes. An LTR-like sequence in the 3' untranslated region. 273 64

The major histocompatibility complex of the rat (RT1 complex) encodes two sets of class II molecules referred to as RT1.B and RT1.D. The complete structure of the RT1.D alpha u chain of the diabetes prone BB rat was determined by the isolation and characterization of a full size cDNA. Comparisons of the nucleotide and protein sequences of RT1.D alpha with the analogous molecules, H-2 I-E alpha and HLA DR alpha, revealed that these alpha chains have been highly conserved during evolution. Southern blot analysis indicated an association of the RT1 haplotypes, 'u' and 'l', with Bam H1 DNA bands of 9.8 kb and 11.7 kb, respectively. The BB rat develops insulin dependent diabetes as an autoimmune abnormality. Accumulating evidence suggests a cellular mediated etiology and the involvement of class II molecules. The steady state levels of RT1.D alpha mRNA were measured in splenic lymphocytes of diabetes prone BB rats and age matched histocompatible normal nondiabetic WF rats by a RNase protection assay. Compared to WF rats, elevated transcripts of RT1.D alpha were found in lymphocytes of young BB rats (approximately 4x and approximately 2.5x greater at 20-40 and 40-75 d, respectively). In lymphocytes of older diabetic and nondiabetic BB rats (greater than 75 d) the levels of RT1.D alpha mRNA were lower than in the young BB rats and were found at the WF control levels. The increased steady state RT1.D alpha mRNA levels in the young BB rats may reflect differences in the proportion of splenic lymphocytes expressing this gene (activated lymphocytes), and thus differences in splenic lymphocyte populations. The steady state RT1.D alpha mRNA levels in lymphocytes of the normal rats were found to be relatively similar at all ages examined. The increased class II gene transcripts found in lymphocytes of young BB rats indicates that they possess a highly activated immune system.
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PMID:The complete sequence of the MHC class II chain RT.1D alpha u of the diabetic BB rat: mRNA levels of RT1.D alpha in lymphocytes. 312 83

A novel mRNA species is specified by the Q6/Q8 gene, a member of the Qa-2-determining family of class-I genes of the murine major histocompatibility complex. It is longer than all previously described class-I transcripts due to an extension at the 3' end of the mRNA past the predicted polyadenylation site. This mRNA was detected by Northern-blot analyses with single or low-copy-number probes to the 3' end of the Q6/Q8 gene. RNase protection experiments have confirmed this finding. The appearance of this mRNA in different strains of mice correlates with the synthesis of the Qa-2 molecule.
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PMID:Novel mRNA species from a Q-subregion class-I gene of the murine major histocompatibility complex. 344 7

We have examined T-cell receptor alpha- and beta-chain variable (V) region gene usage in T-cell populations predicted to have different major histocompatibility complex-restriction specificities. Using a sensitive ribonuclease protection assay to measure T-cell receptor mRNA levels, we found no striking differences in the usage of three V alpha genes and three V beta genes in T-cell populations from three congeneic H-2-disparate strains of mice and between the mutually exclusive Ly2+ L3T4- and Ly2- L3T4+ T-cell subpopulations. These results suggest that major histocompatibility complex restriction cannot be explained by the differential usage of nonoverlapping V alpha or V beta gene pools. In contrast, striking but unpredictable differences were seen in V gene usage in populations of T cells selected by activation with particular alloantigens.
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PMID:T-cell receptor variable region gene usage in T-cell populations. 348 85

Previously we reported that a lethal strain of herpes simplex virus type 2 (HSV-2) infects the brain following ocular inoculation of mice. We now demonstrate that HSV-2 mediates an unusual intracellular sequestering of class II major histocompatibility complex (MHC) antigens. With use of an RNase protection assay, we observed a selective inhibition of IFN-gamma and IL-6 gene transcription in brains of mice infected with HSV-2. It is likely that the inhibition of cytokine gene expression was mediated through a failure to activate CD4+ lymphocytes. These data suggest that the infecting herpesvirus can influence the profile of intracerebrally produced cytokines, which in turn may determine the outcome of the infection.
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PMID:Alteration of intracerebral cytokine production in mice infected with herpes simplex virus types 1 and 2. 796 82


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