Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.31.1 (micrococcal nuclease)
 2,818 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The recent introduction of a reliable, T-lymphocyte proliferation assay, which utilizes thioglycollate-induced, nylon wool column-passed, peritoneal exudate lymphocytes from immune mice (PETLES), allowed us to investigate the genetic control of murine immune responses at the T-lymphocyte level. Examination of the blast cells generated in this population 5 days after stimulation with antigen, revealed that 85% of the cells bore the Thy 1 antigen on their surface, whereas only 5% bore immunoglobulin. Thus, the assay can be considered to measure almost exclusively T-lymphocyte function. This assay was used to examine the T-lymphocyte proliferative responses to seven different antigens: poly(Glu60Ala30Tyr10), poly(Glu58Lys38Tyr4), poly-(Tyr,Glu)-poly-D,L-Ala--poly-Lys, poly-(Phe,Glu)-poly-D,L-Ala--poly-Lys, staphylococcal nuclease, lactate dehydrogenase H4, and the BALB/c IgA myeloma protein, TEPC-15. PETLES from a large number of different inbred mouse strains, including H-2 congenic resistant lines and H-2 recombinants, were studied. The strains could be classified as high responders, low responders, or nonresponders to a particular antigen as judged by the magnitude of the T-lymphocyte proliferative response. In every case but one this classification corresponded to the responder status given the strain based on its ability to mount an in vivo antibody response to the same antigen. For two of the antigens, poly-(Tyr,Glu)-poly-D,L-Ala--poly-Lys and TEPC-15, the immune response genes controlling the T-lymphocyte proliferative response were mapped to the K region or I-A subregion of the major histocompatibility complex, as had previously been shown for the control of the antibody responses to these antigens. This tight linkage of the two phenotypic responses very strongly suggests that the same immune response gene controls the expression of both the proliferative and antibody responses. Since there is essentially no contribution from B lymphocytes in the T-lymphocyte proliferation assay, it seems reasonable to conclude that none of the seven immune response genes studied are expressed solely in B lymphocytes.
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PMID:T-lymphocyte-enriched murine peritoneal exudate cells. II. Genetic control of antigen-induced T-lymphocyte proliferation. 108 91

The recent development of a reliable murine T lymphocyte proliferation assay has facilitated the study of T lymphocyte function in vitro. In this paper, the effect of anti-histocompatibility antisera on the proliferative response was investigated. The continuous presence of anti-Ia antisera in the cultures was found to inhibit the responses to the antigens poly (Glu58 Lys38 Tyr4) [GLT], poly (Tyr, Glu) ploy D,L Ala-poly Lys [(T,G)-A--L], poly (Phe, Glu)-poly D,L Ala-poly Lys [(phi, G)-A--L], lactate dehydrogenase H4, staphylococcal nuclease, and the IgA myeloma protein, TEPC 15. The T lymphocyte proliferative responses to all of these antigens have previously been shown to be under the genetic control of major histocompatibility-linked immune response genes. The anti-Ia antisera were also capable of inhibiting proliferative responses to antigens such as PPD, to which all strains respond. In contrast, antisera directed solely against H-2K or H-2D antigens did not give significant inhibition. Anti-Ia antisera capable of reacting with antigens coded for by genetically defined subregions of the I locus were capable of completely inhibiting the proliferative response. In the two cases studied, GLT and (T,G)-A--L, an Ir gene controlling the T lymphocyte proliferative response to the antigen had been previously mapped to the same subregion as that which coded for the Ia antigens recognized by the blocking antisera. Finally, in F1 hybrids between responder and nonresponder strains, the anti-Ia antisera showed haplotype-specific inhibition. That is, anti-Ia antisera directed against the responder haplotype could completely block the antigen response controlled by Ir genes of that haplotype; anti-Ia antisera directed against Ia antigens of the nonresponder haplotype gave only partial or no inhibition. Since this selective inhibition was reciprocal depending on which antigen was used, it suggested that the mechanism of anti-Ia antisera inhibition was not cell killing or a nonspecific turning off of the cell but rather a blockade of antigen stimulation at the cell surface. Furthermore, the selective inhibition demonstrates a phenotypic linkage between Ir gene products and Ia antigens at the cell surface. These results, coupled with the known genetic linkage of Ir genes and the genes coding for Ia antigens, suggest that Ia antigens are determinants on Ir gene products.
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PMID:T lymphocyte-enriched murine peritoneal exudate cells. III. Inhibition of antigen-induced T lymphocyte Proliferation with anti-Ia antisera. 108 2

This study was conducted in an attempt to characterize some of the effects of sublethal microwave radiation on cells of Staphylococcus aureus. Cultures were exposed to microwave radiation for 10, 20, 30, and 40 s. The effects of a conventional heat treatment were also compared by placing flasks containing cultures in a boiling water bath for the amount of time required to reach temperatures equivalent to those found in cultures exposed to microwave radiation. Control, microwave-treated, and conventionally heat-treated cultures were centrifuged, pellets were resuspended in distilled water, and the resulting suspensions were passed through a French pressure cell. Cell lysates and walls were then isolated and assayed for enzymatic activity. Thermonuclease production was also determined at various levels of exposure of cells to microwave radiation. Activities of malate and alpha-ketoglutarate dehydrogenases, cytochrome oxidase, and cytoplasmic adenosine triphosphatase were higher in microwave-treated cells than in control cells. Membrane adenosine triphosphatase, alkaline phosphatase, and lactate dehydrogenase activities were unaffected when cells were exposed to microwave radiation. The activity of glucose-6-phosphate dehydrogenase was decreased by exposure of cells to microwave radiation. In conventionally heated cells, activities of glucose-6-phosphate and malate dehydrogenases and cytoplasmic adenosine triphosphatase increased activities of alpha-ketoglutarate and lactate dehydrogenases decreased, and alkaline phosphatase activity remained unaffected. Increased levels of thermonuclease activity were observed when cells were exposed to microwave radiation for 10 or 20 s. Data indicate that microwave radiation affects S. aureus in a manner which cannot be explained solely by thermal effects.
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PMID:Comparison of effects of sublethal microwave radiation and conventional heating on the metabolic activity of Staphylococcus aureus. 644 4

Aurintricarboxylic acid (ATA), an inhibitor of Ca(2+)-dependent endonuclease activity, is often used to implicate a role for increased intracellular calcium in mechanistic toxicology studies. We report here on the ability of ATA to inhibit the activity of several NAD(H)/NADP(H)-requiring enzymes (purified or cellular homogenates), including lactic dehydrogenase, alcohol dehydrogenase, cytochrome c reductase, ethoxycoumarin o-dealkylase, isocitric dehydrogenase, glutathione reductase and glucose-6-phosphate dehydrogenase. These results were compared with the ability of ATA to inhibit micrococcal nuclease and rat liver Ca(2+)-dependent endonuclease activity in similar incubations. With the exception of alcohol dehydrogenase, ATA was a potent inhibitor of each of the purified enzymes, with IC50s ranging from 0.5 to 82 microM. In cell homogenates, however, ATA was from 10 to 100-fold less potent at inhibiting these enzymes. When exogenous protein was added to purified enzyme incubations, the effect of ATA was similarly diminished. Our results demonstrate that ATA inhibits a wide range of NAD(H)/NADP(H)-requiring enzymes in in vitro incubations using purified enzymes, but that the inhibitory effects are markedly reduced in incubations which more closely resemble a cellular milieu.
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PMID:Inhibition of NAD(H)/NADP(H)--requiring enzymes by aurintricarboxylic acid. 855 68

The vacuum-ultraviolet circular dichroism (VUVCD) spectra of 16 globular proteins (insulin, lactate dehydrogenase, glucose isomerase, lipase, conalbumin, transferrin, catalase, subtilisin A, alpha-amylase, staphylococcal nuclease, papain, thioredoxin, carbonic anhydrase, elastase, avidin, and xylanase) were successfully measured in aqueous solutions at 25 degrees C from 260 to 160 nm under a high vacuum using a synchrotron-radiation VUVCD spectrophotometer. These proteins exhibited characteristic CD spectra below 190 nm that were related to their different secondary structures, which could not be detected with a conventional CD spectrophotometer. The component spectra of alpha-helices, beta-strands, turns, and unordered structures were obtained by deconvolution analysis of the VUVCD spectra of 31 reference proteins including the 15 proteins reported in our previous paper [Matsuo, K. et al. (2004) J. Biochem. 135, 405-411]. Prediction of the secondary-structure contents using the SELCON3 program was greatly improved, especially for alpha-helices, by extending the short-wavelength limit of CD spectra to 160 nm and by increasing the number of reference proteins. The numbers of alpha-helix and beta-strand segments, which were calculated from the distorted alpha-helix and beta-strand contents, were close to those obtained on X-ray crystallography. These results demonstrate the usefulness of synchrotron-radiation VUVCD spectroscopy for the secondary structure analysis of proteins.
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PMID:Improved estimation of the secondary structures of proteins by vacuum-ultraviolet circular dichroism spectroscopy. 1604 51