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)

In addition to the four major polypeptides VP1 and VP4, foot-and-mouth disease virus particles contain two minor polypeptides, mol. wt. 40 X 10(3) (P40) and 52 X 10(3) (P52). Extensive purification procedures failed to remove these minor polypeptides from the virus particles. Polypeptide P40 co-electrophoresed in SDS-polyacrylamide gels with VP0, the probable precursor of VP2 and VP4 and was inaccessible to iodination in situ. The second minor polypeptide, P52, co-electrophoresed with the virus infection associated (VIA) antigen found in large amounts in harvests of the virus grown in BHK 21 cells. Polypeptide P52 was shown to be located near the surface of the virus particle by iodination experiments and by its removal on incubating the particles with trypsin or chymotrypsin. Pactamycin mapping showed that this polypeptide was not a precursor of the structural polypeptides. About one copy of P52 and 4 copies of P40 were found in the virus particles sedimenting at 146S. However a larger number of copies was found in those virus particles sedimenting faster than the 146S peak.
J Gen Virol 1976 Apr
PMID:Characterization of the minor polypeptides in the foot-and-mouth disease particle. 17 28

Primary human amnion cell monolayers which had been treated with DEAE-dextran, washed, and then inoculated with sonicated cells of the EB3 line of Burkitt's lymphoma cells developed foci of transformed amnion cells 7 to 14 days later. When either the DEAE-dextran or the sonicate was omitted, no significant transformation was found. The foci consisted of enlarging mounds of rapidly dividing cells, which upon subculturing continued their high miotic activity; and strains or lines of the transformed amnion cells were thus readily established. The modal number of chromosomes in such lines was 65 instead of the normal 46. Not all human amnions yielded cells transformable by EB3 cell sonicate, as determined by direct comparisions using the same cultural conditions and testing with the same fresh sonicate preparation in the same experiment. Overall, it appeared that only about 40 to 50% of the amnions yielded transformable cell monolayers; the rest gave monolayers apprently completely refractory to the transformation. The transformed amnion cells contained nuclear and cytoplasmic Epstein-Barr virus (EBV) antigen(s), as revealed by indirect immunofluorescence tests. EB3 cell sonicate also caused the appearance of rapidly growing transformed cell foci on secondary rat embryo cell monolayers which had been sensitized with DEAE-dextran. Calcium in the cell maintenance medium decreased the number of transformed foci found, both on the human and on the rat cell monlayers. Sonicates of cultured normal human leucocytes had no such transforming activity for either the human or the rat cells. The transforming agent in EB3 cell sonicate was completely destructible by either deoxyribonuclease or trypsin, but not by ribonuclease, and was not neutralizable by anti-EBV serum. The simplest interpretation of these results is that the transforming agent is part of all of the EBV DNA plus some necessary protein, with both the DNA and the protein accessible to hydrolytic enzyme action.
J Gen Virol 1976 Jun
PMID:Use of a transfection method to demonstrate a monolayer cell transforming agent from the EB3 line of Burkitt's lymphoma cells. 18 Feb 48

Chymotrypsin cleaves only one of the four major polypeptides of foot-and-mouth disease virus (FMDV serotype O) in situ. This polypeptide (VP1, mol. wt. 29 X 10(3) was first cleaved into fragments of mol. wt. 20 and 9 X 10(3) and further cleavage could be prevented by the addition of a large excess of bovine serum albumin. The infectivity of the virus particles at this stage was the same as that of the intact virus although the rate of attachment to BHK 21 cells was slower and the immunogenic activity was reduced. If hydrolysis was allowed to continue, VP1 was cleaved into fragments with mol. wt. 18 and less than 9 X 10(3), similar to those obtained with trypsin and the virus particles then had a greatly reduced infectivity and a lower immunogenicity. Treatment of strains from five other serotypes of the virus with the two enzymes cleaved only VP1 in each instance and there was a corresponding loss of infectivity. The results are discussed in relation to the location and biological activity of the virus polypeptides.
J Gen Virol 1977 Apr
PMID:Immunogenic and cell attachment sites of FMDV: further evidence for their location in a single capsid polypeptide. 19 41

Exposure of chicken embryo fibroblasts (CEF) to trypsin solubilizes cell surface components, including the initial attachment site for avian tumour viruses (ATV). The soluble attachment site activity appears to interact directly with the ATV in vitro thereby interfering with the binding of at least two ATV subgroups to both intact CEF and CEF plasma membranes. A result of this interaction in vitro is reduced ATV infectivity, demonstrated by reduced transforming capacity of RSV (RAV-I).
J Gen Virol 1977 Nov
PMID:Avian tumour virus interactions with chicken fibroblast membranes: partial characterization of initial attachment site activity. 20 Jul 12

This study investigated the synthesis of membrane antigen (MA) as well as virus capsid antigen (VCA) and early antigen (EA) in Daudi cells which had been superinfected with the P3HR-1 strain of Epstein-Barr virus (EBV) and then treated with trypsin to remove initially absorbed MA-positive material from the cell surface. Synthesis of MA, VCA and EA was completely inhibited by puromycin. A marked reduction in the frequency of MA positive cells was observed in superinfected cells cultured in the presence of either cytosine arabinoside (Ara-C) or phosphonoacetate (PA); however, a small fraction of MA synthesis occurred, suggesting an inhibitor insensitive component in MA, A differential absorption of EBV antibody-positive human serum with the Ara-C treated or untreated infected cells detected two antigenically different components in MA: early (Ara-C insensitive) and late (Ara-C sensitive) MA.
J Gen Virol 1978 Jan
PMID:Appearance of early and late components of Epstein-Barr virus-associated membrane antigen in Daudi cells superinfected with P3HR-1 virus. 20 65

It has been found that 1000-fold more bovine rotavirus is obtained when trypsin is incorporated in the maintenance medium and allowed to remain throughout the growth cycle. This holds true for primary calf kidney (CK) cells and also for several continuous and semi-continuous cell lines. In the presence of trypsin it has been possible to pass the virus serially on continuous cell lines seven times. Concentrations of 1 to 10 microgram/ml of trypsin are found to be effective. Preliminary results suggest that the same technique will be effective for the in vitro propagation of human rotavirus.
J Gen Virol 1978 Jul
PMID:The effect of trypsin on the growth of rotavirus. 21 Nov 80

The structural polypeptides of egg grown mumps virus were analysed by SDS-polyacrylamide-slab-gel electrophoresis. Mumps virions contained eight major polypeptides with mol. wt. of 75, 73, 71, 61, 47, 44, 42 and 40 X 10(3). The 75 K and 61 K polypeptides were glycosylated. In virions treated with pronase and trypsin, the 75 K glycoprotein was removed more readily from the virus than the 61 K glycoprotein. The gradual removal of the 75 K glycoprotein was paralleled by a decrease of haemagglutinating activity. The large glycoprotein was cleaved into a 40 K glycoprotein by trypsin treatment. Pronase and trypsin treatment also removed the smallest 40 K non-glycosylated polypeptide. Thus this polypeptide appears to be located on the outside of the virion and probably represents a cleavage product of the large glycoprotein. Treatment of virions with 2% Triton-X 100 under alkaline conditions in the absence or presence of 2 M-KCl solubilized the two glycoproteins and a fraction of the 71 and 44 K polypeptides, but not the 73 and 47 K polypeptides. The two smallest polypeptides were solubilized by treatment with 2% Triton X-100 in the presence of 2 M-KCl. Since the 40 K polypeptide was interpreted to represent a cleavage product of the large surface glycoprotein the 42 K polypeptide was proposed to represent the membrane protein of mumps virus. The 44 K polypeptide co-migrated with Vero cell actin. The nature of the 47 K polypeptide could not be determined, but it is probably located in the central part of the virus. The 73 K polypeptide and in some experiments also the 71 K polypeptide were found in purified nucleocapsid preparations. It is concluded that mumps virus has a general polypeptide composition similar to other paramyxoviruses. However, the molecular weights of the different polypeptides of mumps virus differ markedly from the corresponding polypeptides in Newcastle disease virus and Sendai virus.
J Gen Virol 1978 Dec
PMID:Structural polypeptides of mumps virus. 21 49

Polyacrylamide gel electrophoresis of bovine rotavirus or neonatal calf diarrhoea virus (NCDV) grown in cell culture resolved eight species of polypeptide. The inner shell particles contained five polypeptides and the outer shell three polypeptides. A major polypeptide of the outer shell was glycosylated. The infectivity of NCDV was enhanced by treatment with trypsin in vitro. All eight polypeptides were affected by trypsin treatment as judged by diminished intensity of polypeptide bands by radiography and several new bands appeared. The intracellular synthesis of NCDV polypeptides was studied by pulse and pulse-chase experiments. Infected cells contained all eight virus capsid proteins and, in addition, three presumably virus-specific polypeptides which were non-capsid polypeptides (NCVP). There was no evidence that any of these polypeptides was processed after synthesis. It is suggested, therefore, that all these polypeptides are primary gene products.
J Gen Virol 1979 May
PMID:Polypeptides of bovine rotavirus. 22 24

Strains of foot-and-mouth disease virus of types O1 and A10 were isolated which showed no significant loss of infectivity upon trypsinization. These 'trypsin-resistant' (TR) viruses were obtained by serial passage in BHK cells of virus that was trypsin-treated before inoculation of the cells. Three O1 isolates were cloned and studied further. Cell attachment of those TR O1 variants (OTR1) was not reduced by trypsinization, unlike that of parent virus. The polypeptide compositions of TR viruses as determined by SDS-polyacrylamide gel electrophoresis were identical with those of parent virus, with the exception of OTR1 which contained an additional polypeptide approx, 3000 daltons larger than VP1. After trypsinization, which normally cleaves VP1, the polypeptide composition of the three TR viruses (including OTR1) and of parent virus did not show any significant difference. In OTR1 both the additional virus protein and VP1 were cleaved into a P18 molecule and smaller fragments. The surface location of this additional polypeptide was confirmed by iodination experiments. It was shown by immunodiffusion experiments that only OTR1 differed from the parent virus. This antigenic change was present on the trypsin-sensitive part of the virus since trypsinized TR viruses (including OTR1) were antigenically identical to trypsinized parent virus. The electrophoretic mobilities of the three OTR viruses isolated, and of parent virus, differed somewhat before trypsinization. After trypsin-treatment, the mobilities of TR viruses were all increased to the same level; however, their rate of migration was lower than that of trypsin-treated parent virus. This lower mobility of trypsin-treated OTR viruses was the only difference which could be associated with retained infectivity.
J Gen Virol 1979 May
PMID:Isolation and characterization of trypsin-resistant O1 variants of foot-and-mouth disease virus. 22 25

A sensitive, quantitative and reproducible plaque assay for the measurement of the simian rotavirus SAII is described. Plaque formation required the presence of the facilitators pancreatin or trypsin and diethylaminoethyl-dextran in the agar overlay. SAII produced plaques in three continuous primate cell lines: MA-104, CV-1 and LLC-MK2. MA-104 cells were the most sensitive.
J Gen Virol 1979 Jun
PMID:A plaque assay for the simian rotavirus SAII. 22 32


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