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:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chicken eggs at embryonation day (ED) 18 or newly hatched chicks were inoculated with turkey herpesvirus (HVT), Marek's disease virus (MDV), or virus-free diluent and, at intervals after inoculation, tissue homogenates of virus-exposed and virus-free chickens or chicken embryos were examined for interferon (IFN) activity. Homogenates of lung, thymus and spleen specimens from chickens given HVT at ED 18 had IFN activity. Activity of IFN in the lungs was studied further. Homogenates of lung specimens from chickens exposed to HVT at hatching also had IFN activity, although the concentration of IFN was lower than that in chickens given HVT at ED 18. The pathogenic isolates of MDV (JM-MDV), but not the attenuated (Md11/75C-MDV) or nonpathogenic (SB1-MDV) isolates, inoculated at ED 18 also induced high lung IFN activity. Exposure to a combination of HVT and SB1-MDV induced IFN activity comparable with that in chickens given HVT alone. The IFN activity in homogenates of lung specimens from virus-exposed chickens was species specific and heat and pH stable, but was destroyed by trypsin treatment. Occasionally, low IFN activity also was detected in homogenates of tissue specimens from virus-free chickens or chicken embryos. This IFN activity could have been produced constitutively or may have been induced by substances (inducers) in the environment.
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PMID:In situ production of interferon in tissues of chickens exposed as embryos to turkey herpesvirus and Marek's disease virus. 247 45

Influenza virus strain A/USSR/053/74/H3N2 was subjected to the effect of soluble and nonsoluble trypsin. Both enzymes appeared to affect the activity of neuraminidase. The viruses altered in this way did not induce interferon (IFN) in mice. Treatment of viral particles with soluble bromeline brought about almost complete inactivation of hemagglutinin and slight suppression of neuraminidase activity. This virus was capable of IFN induction. On the other hand, when nonsoluble bromeline was used as the treatment agent, complete inactivation of neuraminidase and reduction of hemagglutinin titer were observed. This virus was not capable of IFN induction. Viral preparations treated with pronase, trypsin and bromeline for a total extraction of the surface antigens, did not induce IFN. The viruses treated with these enzymes were examined under the electron microscope. Trypsin-treated viruses showed no changes on their surface while bromeline and pronase totally extracted the spikes of surface antigens.
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PMID:Ultrastructure and some biological properties of influenza A virus. IV. Effect of proteolytic enzymes on viral particle. 247 2

The replication of Moloney murine leukemia virus (MMuLV) in chronically infected mouse cells arrested at the G0/G1 phase of the cell cycle by different procedures was investigated. MMuLV production was inhibited in glutamine- and isoleucine (Gln-Ile)-deprived G0/G1 cells. In contrast, butyric acid treatment, which efficiently arrested the cells at the G0/G1 phase of the cell cycle, did not inhibit MMuLV production. Furthermore, the inhibition of MMuLV production caused by either Gln-Ile deprivation or by interferon (IFN) treatment was overcome by butyric acid treatment. Thus, the replication of MMuLV could be dissociated from cell proliferation. The inhibition of MMuLV production in Gln-Ile-deprived cell cultures was compared to the inhibitory effect of IFN, which is known to affect budding and release of the virus. Rates of MMuLV protein synthesis were not affected in both the IFN-treated and Gln-Ile-deprived cells. However, processing of the viral polyprotein Pre65gag into p30 was blocked in the Gln-Ile-deprived cells. Furthermore, whereas in IFN-treated cells, MMuLV accumulated on the cell surface and could be released upon treatment with trypsin, in Gln-Ile-deprived cells, no virions were released by such treatment. These results indicate that in cells arrested by Gln-Ile deprivation, MMuLV is inhibited at a posttranslation step. This step appears to precede the anti-MMuLV block induced by IFN.
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PMID:Regulation of Moloney murine leukemia virus replication in chronically infected cells arrested at the G0/G1 phase. 258 48

The 76-kd human interferon (IFN)-induced MX protein is the homolog to the murine protein, which is necessary and sufficient to provide adequate resistance to influenza virus infection in murine cells and in mice. Fifty-one patients with systemic lupus erythematosus (SLE) were screened for the presence of the MX homolog in mononuclear cells and for IFN and anti-IFN antibodies in serum. In 47 of 51 patients, significant levels of the MX homolog were found, while only 15 of 51 patients had measurable alpha-IFN in their serum. The IFN activity found in these sera was characterized as a partially acid-labile alpha-IFN, by means of acid-stability cross-reactivity on heterologous cells, trypsin sensitivity, and neutralization by homologous or heterologous antisera. Four of the patients had no detectable MX homolog in their leukocytes; 3 of these 4 possessed an anti-alpha-IFN antibody that was able to neutralize both a natural alpha-IFN preparation and the acid-labile IFN in SLE sera. Also, acid-labile alpha-IFN-containing SLE sera induced the MX homolog in vitro in mononuclear cells from healthy donors. These observations suggest that endogenously produced alpha-IFN is responsible for the observed induction of the MX homolog in SLE and that the IFN system is activated in more than 90% of SLE patients.
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PMID:MX homologous protein in mononuclear cells from patients with systemic lupus erythematosus. 275 23

Neurotropic coronavirus (mouse hepatitis virus strain A59) infection induces major histocompatibility complex class I (H-2) surface antigens on oligodendrocytes and astrocytes, cells that do not normally express detectable MHC antigens on their surface. The induction on MHC antigen expression potentially allows immunocytes to interact with infected glial cells and may play a critical role in the development of virus-induced, immune-mediated demyelination in the central nervous system, a possible model of human multiple sclerosis. In this study, we characterized the soluble factor involved in MHC antigen induction, quantitated induction of MHC antigens, and analyzed the central nervous system cell type involved in the production of the factor. The H-2-inducing factor, most likely produced by astrocytes, was found to be nondialyzable, heat- and trypsin-sensitive, but resistant to treatment at pH 2.0. The m.w. of the factor was estimated as 50 to 100 kDa. Studies on fractionation by ultrafiltration and sucrose density gradient along with antibody-blocking experiments indicate that the factor is not interferon or virus particles.
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PMID:Induction of glial cell MHC antigen expression in neurotropic coronavirus infections. Characterization of the H-2-inducing soluble factor elaborated by infected brain cells. 283 Dec 79

Natural bovine leukocyte interferon (IFN) was produced in high titer (15,314 U/ml), with Sendai virus as the inducer at 300 hemagglutinating units (HA)/ml and 12 h incubation. Its antiviral activity was completely stable for 30 days at 4 degrees C, -20 degrees C, or -70 degrees C, and 96 h at 37 degrees C, but some activity was lost after 15 min at 56 degrees C. All activity was lost after treatment with trypsin, but pH 2.0 dialysis had no effect. Bovine leukocyte IFN inhibited growth of bovine kidney cells in tissue culture. The system reported could be used to produce bovine leukocyte IFN in quantities sufficient for clinical use in cattle.
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PMID:Bovine leukocyte interferon: characterization and large-scale production. 283 18

In the present study we have evaluated the effect of recombinant human fibroblast, IFN-beta ser, and immune, IFN-gamma, interferon, alone and in combination, on the proliferation of fifteen early passage human glioblastoma cell cultures. Explant cultures were established from glioblastoma tumor tissue obtained at the time of surgery. After sufficient outgrowth, cultures were dispersed with trypsin/versene and maintained as independent cell lines. IFN-beta ser induced a greater than or equal to 50% reduction in the 7 day growth of 6 of the 15 cultures. The majority of cultures, 9 of 15, displayed less than or equal to 50% growth suppression in comparison with control cultures after 7 days exposure to 2000 Units/ml of IFN-beta ser. When treated with 2000 Units/ml of IFN-gamma, only 1 of the 15 glioblastoma cultures exhibited a greater than or equal to 50% reduction in growth. In contrast, when treated with the combination of IFN-beta ser plus IFN-gamma, 1000 Units/ml of each interferon preparation, 12 of 15 cultures were inhibited by greater than or equal to 50% after 7 days growth. The combination of interferons was effective in suppressing glioblastoma growth both in cultures displaying relative sensitivity and those exhibiting innate resistance to either or both types of interferon when employed alone. One glioblastoma culture, G-7, was studied through 45 passages and displayed the same sensitivity at different passages to growth inhibition when exposed to IFN-beta ser, IFN-gamma or both interferons. Based on previous clinical studies indicating that IFN-beta or IFN-gamma when administered alone to patients do not generally alter the clinical progression of malignant gliomas, the present results suggest that the combination of IFN-beta plus IFN-gamma may prove more effective than either agent alone in the clinical treatment of patients with glioblastoma multiforme.
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PMID:Enhanced in vitro growth suppression of human glioblastoma cultures treated with the combination of recombinant fibroblast and immune interferons. 283 97

Human retroviruses have recently been linked with T cell lymphoproliferative disorders and with the acquired immune deficiency syndrome. We investigated the mechanisms for acquired pure red cell aplasia and cutaneous anergy in a patient with the chronic T gamma-lymphoproliferative disease (T gamma-LPD) syndrome. Patient marrow erythroid progenitors (BFU-E) were 17 +/- 9% of control and were selectively increased to 88-102% of control after marrow T cell depletion. Patient Leu 2+ suppressor T cells spontaneously produced high titers of human gamma-interferon and resulted in a concentration-dependent selective inhibition (74-91%) of BFU-E when co-cultured with autologous or allogeneic marrow. Conditioned media (CM) derived from patient Leu 2+ T cells similarly inhibited growth of autologous or allogeneic marrow BFU-E. The inhibitory factor derived from patient CM was acid-labile (pH 2) and sensitive to trypsin; prior treatment of patient T cells with anti-HLA-DR monoclonal antibody plus complement abrogated the suppressive effect of T cell-derived CM. Patient peripheral blood mononuclear cells (PBMC) were unable to support growth of cultured interleukin 2 (IL 2)-dependent T cells, but responded to exogenous IL 2 in vitro with a 16-21-fold augmentation, relative to control, in mitogen-induced proliferation. Antibodies to HTLV-I core proteins p19 and p24 but not to HTLV-III proteins were detected in patient serum by Western blotting; patient cultured PBMC stained (7-11%) with antibodies to p19 and p24. Patient cultured PBMC demonstrated integrated HTLV-I genomic sequences by the Southern technique and expressed both specific HTLV-I genomic sequences by RNA dot blot plus reverse transcriptase activity. Utilizing a cloned DNA probe for the beta chain of the T cell receptor gene, patient PMBC demonstrated gene rearrangements providing presumptive evidence for clonality. The presence in serum of HTLV-I p19 and p24 antibodies, the expression of p19 and p24 core antigens on patient mononuclear cells, the evidence of HTLV-I proviral integration sequences and the expression of HTLV-I genomic sequences in patient cells, indicates infection with HTLV-I and raises the possibility of an etiologic link between human retrovirus infection and some instances of large granular lymphocytic leukemia (T gamma-LPD).
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PMID:Human T cell leukemia virus-I-associated T-suppressor cell inhibition of erythropoiesis in a patient with pure red cell aplasia and chronic T gamma-lymphoproliferative disease. 289 60

The culture supernatant (SN) from a cloned line of thymic stroma-derived cells in fibroblastic form (TSCF) contained a factor capable of supporting the growth of the interleukin (IL) 2-dependent, antigen-specific helper T cell (Th) clone 9-16 without requiring IL2 and antigen. This active substance, designated as thymic stroma-derived T-cell growth factor (TSTGF), was partially purified through DEAE-Sephacel chromatography and PBE 94 chromatofocusing. The original SN did not contain IL1, IL2, IL3, IL4, or interferon activities; but an appreciable magnitude of colony-stimulating factor (CSF) activity in addition to TSTGF was present, whereas the partially purified preparation of TSTGF was depleted of any type of CSF activity. The elution profile of TSTGF activity on the chromatofocusing has revealed that TSTGF has an isoelectric point (pI) of about 6.0. When a purified TSTGF sample was applied to Sephacryl S-200 column chromatography and sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis, TSTGF activity was eluted in a single peak around an apparent molecular weight of about 25,000. The activity of TSTGF also was shown to be relatively stable with heat treatment and in the wide range of pH, but it was abolished by treatment with either trypsin or dithiothreitol. These results indicate that TSTGF, a novel T-cell growth factor, is the protein that has an apparent molecular weight of about 25,000 and a pI of 6.0, and in the intact molecule, it contains the disulfide bond(s) required to maintain and/or express its biologic activity.
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PMID:Thymic stroma-derived T-cell growth factor (TSTGF): II. Biochemical and functional characterization. 304 41

Sera from mice which have been vaccinated with BCG and challenged with old tuberculin contain gamma interferon. These same sera also express antibacterial activity. Using Staphylococcus aureus we demonstrated that its growth was inhibited at dilutions of sera as high as 1:320. A 4% concentration of sera reduced the growth rate of the S. aureus from 1.6 to 0.6 doubling times per hour. The activity was stable at 56 degrees C but destroyed by 80 degrees C. It was nondialysable and destroyed by acid conditions (pH 2.0) and by the proteolytic enzymes trypsin and chymotrypsin. Antibodies to gamma interferon neutralized the antiviral activity but not the antibacterial activity. Mitogen-induced and virus-induced interferons did not have activity. We subsequently demonstrated that the factor could be induced in mice using BCG without the secondary old tuberculin challenge. No gamma interferon was found in the sera of mice given BCG without old tuberculin. These findings indicate that the antibacterial activity of these sera is not dependent on the presence of gamma interferon. We will continue to work to characterize and identify the antibacterial component in these sera.
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PMID:Antibacterial activity of BCG-induced, interferon-containing sera. 308 10


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