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)

Endogenous factors inhibiting the proliferation of T-lymphocytes were investigated which may function as modulators of T-lymphocyte production within the thymus. An extract from calf thymus (T4) enriched in lymphocyte chalone arrests rat thymocytes at the G1 leads to S boundary and in the S phase of the cell cycle in short-term cultures. It also inhibits the proliferative response of human peripheral blood lymphocytes to PHA-P in a time-dependent manner, as well as the spontaneous proliferation of in vitro cultured human chronic leukaemic lymphoblasts. This crude extract contains two active moities which can be isolated by molecular filtration on Sephadex G-75 column. A species non-specific, cell line selectivity inhibitory effect is characteristic of the high molecular weight fraction (mol. wt. greater than 40,000). This activity is resistant to moderate heat treatment and trypsin but is sensitive to mild alkaline hydrolysis and to RNase A digestion. About ten protein components and a toluidine blue positive substance can be detected by analytical polyacrylamide gel electrophoresis. The active inhibitor, a proposed protein-RNA complex, might be identical with the chalone. The low molecular weight, non-dialysable factor (T4-4) inhibits [3H]thymidine incorporation into acid insoluble DNA in a cell non-specific manner. A possible relationship between the two activities is discussed.
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PMID:Endogenous thymic factors regulating cell proliferation and analysis of their mechanism of action. 14 69

The cloning potential of PHA-treated T cells is significantly enhanced when lymphocyte culture fluid (LCF) from mitogen-treated lymphocytes is added to the soft agar culture system. The mitogens seem to stimulate the release of a lymphocyte colony enhancing factor (LCEF) into the culture medium. A study of the physico-chemical properties of the LCEF revealed that it is a nondialyzable, heat-labile molecule which migrates in the haptoglobin (2--2) post-transferrin region in acrylamide electrophoresis. It is stable to RNase and DNase but labile to papain and trypsin. The LCEF was partially purified from the crude LCF using a sequence of techniques--ammonium sulphate precipitation, DEAE-cellulose and Bio-Gel P-150 chromatography and disc electrophoresis. The mol. wt of the purified LCEF, determined from gel filtration chromatography, was 90,000--110,000.
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PMID:Partial purification and characterization of the human lymphocyte colony enhancing factor (LCEF). 30 93

The carboxymethylated, oxidized and reduced forms of AS RNase inhibited transplantability and DNA synthesis of tumour cells BP-8 and EL-4 incubated in vitro. With tumour cells EL-4 the results under in vitro conditions did not not correspond to those obtained under the conditions in vivo. The survival of mice given injections of EL-4 cells and of the native and carboxymethylated AS RNase was only slightly prolonged. Mice that received intra-abdominally BP-8 cells and both carboxymethylated and oxidized and reduced forms of AS RNase survived two or three times longer than the controls. Succinylation and maleylation of AS RNase eliminated any antitumoral effect. Aspermatogenic activity of AS RNase was abolished by any modification of the molecule which had substantially reduced, or removed, the RNase activity. Neither native nor modified forms of AS RNase had an inhibitory effect on unstimulated pig lymphocytes. The DNA synthesis of PHA-stimulated lymphocytes was inhibited by the native and carboxymethylated AS RNase only. Bovine pancreatic A RNase had any inhibitory effect on neither tumour nor testicular cells.
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PMID:Effect of native and modified bull seminal ribonuclease on tumour and testicular cells and phytohaemagglutinin-stimulated pig lymphocytes. 37 93

Tumor culture toxohormone (TCT) obtained from cultures of MBQA mouse tumor cells, a line derived from a methylcholanthrene-induced fibrosarcoma (CBA/J origin), suppressed the mitogenic responsiveness of mouse spleen cells (PHA, LPS) as well as the antibody formation to SRBC in vitro. The immunosuppressive activity of toxohormone was readily inactivated by heating at 100 degrees C or treatment with trypsin, but not by DNase and RNase treatment.
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PMID:Immunosuppression induced by "toxohormone" from mouse tumor cells in culture. 49 45

Addition of increasing concentrations of autologous DNA, but not of allogeneic DNA, in culture media of human lymphocytes induces a parallel increase of thymidine incorporation into leucocytes and of lymphocytes transformation into blast cells. Specificity of DNA action was analysed by different DNase and RNase treatments. DNase or RNase alone neither stimulates blastic transformation of lymphocytes and incorporation of thymidine into leucocytes, nor inhibits PHA-induced stimulations of these cells. However Dnase--but almost not RNase--clearly inhibits thymidine incorporation and blast transformation induced by autologous DNA.
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PMID:Stimulation of human lymphocytes in vitro by purified autologous DNA. 86 12

Supernatants from PHA-activated human peripheral blood mononuclear cells, depleted of virtually all IL-2 activity by an anti-rIL-2 immunoadsorbent column, contain a factor(s) which synergizes with rIL-2 in facilitating the generation of allogeneic human CTL responses in vitro. This factor, provisionally termed CTL maturation factor (TcMF), did not appear to promote CTL responses in the absence of rIL-2. Furthermore, it acted later than IL-2 in facilitating CTL responses and could not be replaced by recombinant IFN-gamma. In this report we show that rIFN-alpha, rIL-1 alpha, and rIL-1 beta likewise lack TcMF activity. The TcMF activity in lymphokine-containing culture supernatants could be eliminated by trypsin or pronase but not by neuraminidase or RNase. Gel filtration revealed two peaks of TcMF activity, one at 12,000 to 25,000 Da and the other at 45,000 to 65,000 Da. Isoelectrofocusing demonstrated substantial charge heterogeneity. The majority of TcMF activity was recovered between pI 4.0 and pI 5.5 with a minor component at pI 6.5, corresponding to the areas in which IL-1 activity was also found. However, TcMF activity could be separated from IL-1 by reverse-phase HPLC. Moreover, TcMF recovered following reverse-phase HPLC was also found to be depleted of IL-4 activity. These studies suggest that TcMF activity is mediated by a protein(s) distinct from IL-1, IL-2, IL-4, and interferon-alpha or-gamma.
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PMID:Characterization of a factor(s) which synergizes with recombinant interleukin 2 in promoting allogeneic human cytolytic T-lymphocyte responses in vitro. 327 3

Cancer grows in interaction with the host, that is, a host-tumor relationship exists. Investigations of host factors in patients receiving cancer chemotherapy are important, as they reveal the conditions in which a tumor response can develop. Furthermore, reliable host factors, if present, will be useful for quantitative evaluation of the effects of treatment. We have investigated the following three categories of host factors in relation to the effects of cancer chemotherapy and/or immunotherapy. CBC, and blood chemistries (44 parameters). Tumor markers; sialic acid, RNase, lysozyme, ferritin, IAP (immunosuppressive acidic protein), elastase I, AFP, CEA, POA, CA 19-9, CA 125, etc. Immunological parameters; lymphocyte, active T cell, T cell, B cell, IgG Fc receptor-positive T cell, lymphocyte blastogenesis stimulated by PHA, or concanavalin-A, ADCC activity, interferon production in vitro induced by poly I: C, or PHA, PPD skin test, immune complex, immunoglobulin G, A, and M, OKT series 3, 4, 8, 11, 4/8 ratio, antihuman HLA-DR, Leu 11, NK cell activity, etc. From our clinical observations, there were no significant differences in the pretreatment levels of these parameters between responders and non-responders. In responders, there was a tendency for the host factors to show greater degrees of improvement following treatment than in non-responders, but none proved to be reasonably reliable parameters for evaluating therapeutic effects. On the other hand, from our clinical observations on the advanced gastric cancer cases, life span showed a close correlation with tumor regression induced by cancer chemotherapy. Because of these facts, it is only natural that the clinical effects of chemotherapy are currently determined by definite tumor regression.
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PMID:[Host factors in cancer chemotherapy]. 372 33

The native dimer bovine seminal ribonuclease, AS RNase, and its four modified derivatives (carboxymethylated, succinylated, oxidated and reduced) were examined for their effects on PHA- or PWM-stimulated human lymphocytes, mixed lymphocyte cultures and lymphoblastoid cell line line (Molt-3, RAJI, UHKT-2 and UHKT-5). Among all substances tested the native AS RNase exerted the strongest suppressive effect on PHA-, PWM-, and MLR- stimulated lymphocytes. At concentrations of 5 and 100 microgram/ml AS RNase inhibited lymphocyte stimulation in MLR by 40 and 95%. The carboxymethylated and reduced derivatives possessed inhibitory effect one order lower, while the succinylated derivative showed a negligible effect, and the oxidated derivative was ineffective. The inhibitory effect on PHA-stimulated lymphocytes was not reduced when AS RNase was added to lymphocyte culture 24 or 48 h later. Likewise, the 20-fold increase in PHA concentration did not cause any decrease in inhibitory effect of AS RNase. AS RNase added to transformed lymphocytes simultaneously with 3H-TdR did not affect the thymidine uptake. As RNase also had the strongest inhibitory effect on growth, viability and the DNA synthesis in all lymphoblastoid cell lines tested. After 72 h cultivation with AS RNase at a concentration of 100 microgram/ml, the DNA synthesis decreased by more than 90% in Molt-3 and UHKT-2 cells. Simultaneously reduction in cell count and increased numbers of dead cells compared to control cultures were found. Carboxymethylated derivative at the same concentration inhibited thymidine incorporation into the DNA by 70% but did not cause any cytotoxic effect. Other derivatives showed negligible or null effects. These results are in agreement with some data published earlier, that the dimer of seminal ribonuclease exerts a significant antitumour effect. The immunosuppressive effects of AS RNase observed in the present paper suggest that this compound is one of the components of seminal plasma which may take part in suppression of immune responses of the female reproductive tract to spermatozoa.
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PMID:Inhibitory effect of bovine seminal ribonuclease on activated lymphocyte and lymphoblastoid cell lines in vitro. 645 59

We have re-examined whether pp60c-src, the normal cellular homologue of the transforming protein of Rous sarcoma virus, is present in human T cells. By in vitro immune-complex kinase assay or Western blotting with the anti-pp60c-src mAbs 327 or GD11, pp60c-src was found to be present in lysates of T cell lines, including the Jurkat T cell line. The 327 and GD11 mAbs have been reported to be specific for pp60c-src and not to cross-react with other src family members or other kinases. Furthermore, the size of the pp60c-src bands present on Western blotting and in vitro kinase assay were clearly different from those of p56lck or p59fyn. In addition, pp60c-src is detected in the HTLV-I-derived T cell lines S1T and C8, which lack expression of p56lck and p59fyn. RNase protection assays confirmed that pp60c-src mRNA is present in Jurkat T cells. We also found pp60c-src protein to be constitutively present in freshly isolated thymocytes. In contrast, pp60c-src was absent, or present at extremely low levels, in normal, resting peripheral blood T lymphocytes, which is in agreement with previous findings. However, after stimulation of resting T cells with the mitogenic lectin PHA or with Ab to the TCR complex, pp60c-src expression is induced in both CD4+ and CD8+ T cell subsets, with peak expression detectable 12 to 24 h after T cell activation. The levels of pp60c-src are low in all T cells except Jurkat, where levels of pp60c-src are comparable to levels found in a glioblastoma cell line (T98G). Nevertheless, significant levels of pp60c-src kinase activity are readily detectable in thymocytes and activated normal T cells as well as in T cell lines. The finding that pp60c-src is inducible following activation through the TCR suggests that pp60c-src may play a specific role in the normal T cell activation pathway.
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PMID:pp60c-src expression is induced by activation of normal human T lymphocytes. 753 11

In this study, we have analyzed the expression and regulation of receptors for IL-2 (alpha and beta chains) and IL-4 in four lymphoid cell lines established from leukemic cells. The gibbon ape cell line MLA 144 was the only one to express constitutively the IL-2R beta chain and IL-4R, whereas the NK-like YT cells express only IL-2R beta. The two other cell lines in this study, PEER and HSB2, are derived from T lymphocytes, and express neither IL-4R, IL-2R beta, nor IL-2R alpha unless stimulated. We report here that those receptors that are constitutively expressed, i.e., IL-2R beta on YT cells and IL-2R beta or IL-4R on MLA cells, are down-regulated by stimulation with PHA + PMA. In contrast, RNase protection experiments showed that PHA + PMA stimulation of T cell lines induces mRNA for all three receptors in PEER cells, and only IL-2R alpha and IL-4R in HSB-2. Thus each of these three receptors is subjected to a different regulation, which in addition varies depending on the lineage (or differentiation stage) of the cells. This was further supported by the finding that IL-1 alpha or TNF-alpha regulates these receptors differently. These two cytokines have no effect on IL-2R beta and IL-4R in MLA and YT, but induce IL-2R alpha in YT. In contrast, they do not induce either chains of the IL-2R in the T cell lines PEER or HSB-2, but TNF induces IL-4R mRNA in HSB2 cells, and IL-1 does so in both cell lines.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of interleukin-2 and interleukin-4 receptor expression in human and ape lymphoid cell lines. 845 29


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