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)

A papovavirus, CCL 33 PV, isolated from a porcine cell line, CCL 33 (GT), was characterized. Based on a comparison of four isoenzyme systems, CCL 33 (GT) and CCL 33 (ATCC), obtained directly from the American Type Culture Collection, appeared to be the same. In addition to the previously characterized C-type virus of CCL 33 cultures, CCL 33 (GT) produced CCL 33 PV in high quantity, but CCL 33 (ATCC) produces a papovalike virus, presumably the same as CCL 33 PV, in barely detectable amounts. Serological results showed that CCL 33 PV is apparently identical to a papovavirus (SPV) isolated by Newman and Smith after inoculation of CCL 33 with concentrated porcine trypsin. These studies extend the characterization of this papovavirus, demonstrating that CCL 33 PV is weakly hemagglutinating after neuraminidase treatment, has a high affinity for a component of fetal bovine serum and is highly infectious in appropriate porcine cell systems rather than very defective as reported previously. Moreover, it was concluded from the data that CCL 33 PV is probably indigenous to the CCL 33 porcine cell line.
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PMID:Concurrent replication of a papovavirus and a C-type virus in the CCL 33 porcine cell line. 23 60

125I-labelled alpha 2-macroglobulin complexed with trypsin bound to human cancer cell lines (HTB 144, CRL 1427, CCL 30, HB 8065, CCL 2, CRL 1593) but to a lesser degree than to normal cells. Malignant transformation of murine BALB/c 3T3 cells with Kirsten sarcoma virus caused a 50% reduction in the alpha 2-macroglobulin-trypsin complex binding. Two cloned revertants derived from the malignant BALB/c 3T3 cells did not induce tumors upon syngrafting. One exhibited normal binding and the other reduced binding. A reduced alpha 2M-proteinase complex binding is thus common in tumor cells but is not a unique property of the malignant state.
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PMID:Low alpha 2-macroglobulin-proteinase complex binding: a common but not exclusive characteristic of malignant cells. 248 39

Effects of human recombinant-DNA derived interferon-gamma and -alpha 2 on the adhesion of cultured breast cancer cells (BT-20, ZR-75.1, MCF-7, 734-B and Hs-578-T), larynx carcinoma cells (HEP-2), epidermoid carcinoma cells (KB), lung carcinoma cells (CCL 185), and ovarian carcinoma cells (1847) to the surface of cell culture plastic dishes were studied. Layered cells were detached after a 3-day treatment with interferon either by trypsin-EDTA, trypsin, protease or cooling to 4 degrees C. Treatment with interferon-gamma (500 unit/ml) significantly increased the incubation time for trypsin-EDTA, EDTA and at 4 degrees C necessary to bring cells into suspension for the 4 cell lines BT-20, ZR-75.1, MCF-7 and HEP-2. Interferon-alpha 2 was not able to induce a similar effect. Reattachment of interferon-gamma treated ZR-75.1 cells was not increased after harvesting by trypsinization or EDTA action. Decreased adhesion of cultured cells is associated with transformation and the effects of interferon-gamma may be explained by reinforced normal phenotype. Interferon-gamma induced adhesion was not associated with other interferon effects especially the anti-proliferative activity or modulation of surface antigens.
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PMID:Human interferon-gamma increases adhesion of cultured carcinoma cells to the substratum. 311 53

The cell surface glycopeptides from an epithelial cell line (CCL 239) derived from normal human colon were compared with those from three cell lines (HCT-8R, HCT-15, and CaCo-2) derived independently from human colonic adenocarcinomas. Cells were incubated with D-[2-3H]mannose or L-[5,6-3H]fucose for 24 h and treated with trypsin to release cell surface components which were then digested exhaustively with Pronase and fractionated on Bio-Gel P-6 before and after treatment with endo-beta-N-acetylglucosaminidase H. The most noticeable difference between the labeled glycopeptides from the tumor and CCL 239 cells was the presence in the former of an endo-beta-N-acetylglucosaminidase H-resistant high molecular weight glycopeptide fraction which was eluted in the void volume of Bio-Gel P-6. This fraction was obtained with both labeled mannose and fucose as precursors. However, acid hydrolysis of this fraction obtained after incubation with [2-3H]mannose revealed that as much as 60-90% of the radioactivity was recovered as fucose. Analysis of the total glycopeptides (cell surface and cell pellet) obtained after incubation with [2-3H]mannose showed that from 40-45% of the radioactivity in the tumor cells and less than 10% of the radioactivity in the CCL 239 cells was recovered as fucose. After incubation of the HCT-8R cells with D-[1,6-3H]glucosamine and L-[1-14C]fucose, strong acid hydrolysis of the labeled glycopeptide fraction excluded from Bio-Gel P-6 produced 3H-labeled N-acetylglucosamine and N-acetylgalactosamine. This high molecular weight glycopeptide fraction was susceptible to mild alkaline borohydride reduction, yielding a mixture of labeled oligosaccharides which contained N-acetylgalactosaminitol. Thus, the HCT-8R cells are expressing fucosylated mucin-type glycoproteins on their surface.
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PMID:Cell surface glycopeptides from human intestinal epithelial cell lines derived from normal colon and colon adenocarcinomas. 405 24

Karyotypes of nine human colorectal cell lines deposited with the ATCC were studied by trypsin-Giemsa banding. CCL 229,230,231 and 235 (Modal chromosome number, Sm, was 49, 68, 47, and 40, respectively) belong in the stable type that is characterized by karyotypes consisting mostly of normal chromosomes and stable markers. CCL 228, 234, and 238 (Sm=55,79, and 70 respectively) belong in the unstable type that has karyotypes consisting of numerous markers in addition to normal chromosomes and stable markers. The remaining intermediate type (CCL 233 and 237, Sm = 60 and 64, respectively) has karyotypic characteristics between the above two types usually with two or less unstable markers per cell. The stable markers (together with normal chromosomes) are constitutive components of a cell genome and are common to most cells within the same cultured population. Unstable markers, which generally constitute only a small portion of the total chromosome complement are the likely cause of karyotypic variations between cells and often are produced by balanced inter- or intrachromosome changes, or both. Consequently, total chromosome length per cell genome is remarkably consistent within a cell population, and karyotypes between cells, such as from four stable lines, are profoundly stable and mostly identical. Chromosome deletions and interhomologue exchanges (including isochromosomes) had the highest incidences among both stable and unstable markers. The complex markers occurred relatively infrequently. There were neither common markers nor unique chromosome breakages common to all of these established cell lines. However, chromosomes No. 7 and 1 had the highest incidence (15 and 12, respectively) of structural modifications resulting in the formation of stable markers (82 total exchanges in nine cell lines), and chromosomes No. 7 and 2 were involved at high incidence (21 and 15, respectively) in the formation of both stable and unstable markers (181 total exchanges). Moreover, No. 7 is overrepresented in eight of nine lines. The significance of chromosome changes involving No. 7 in this as well as other tumor pathotypes is briefly discussed.
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PMID:Karyotype consistency in human colorectal carcinoma cell lines established in vitro. 710 89

Several inbred strains of mice in closed breeding colonies were found to have spiral-shaped bacteria associated with active, chronic hepatitis. A new species of Helicobacter, H. hepaticus, was isolated from the infected livers of some strains of mice. Other strains of mice were colonised with H. hepaticus in the caecum and colon, but not the liver. Filtersterilised supernatant fluid from five strains of H. hepaticus was tested in a mouse liver cell line (ATCC no. CCL 9.1) for cytotoxic activity. All strains produced a toxic factor causing morphological changes in the cells at dilutions up to 1 in 1000. Toxicity was observed after exposure to the supernatant fluid for 48-72 h. Other Helicobacter spp. that also produced the cytopathic effect (CPE) in the liver cell line were H. felis, H. acinonyx, H. pylori and one strain of H. mustelae. "Helicobacter rappini" and H. muridarum did not cause CPE in the liver cells. The soluble factor was stable at 4 degrees C for up to 3 months. It was also stable at 56 degrees C for 30 min, but was inactivated by boiling for 15 min. It was inactivated by incubation with trypsin. A partially purified preparation of the cytotoxin had a mol. wt of c. 100,000 and did not have urease activity. The cytotoxin produced by H. hepaticus did not cause vacuole formation in HeLa cells.
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PMID:In-vitro hepatotoxic factor in Helicobacter hepaticus, H. pylori and other Helicobacter species. 773 25

Perigraft fluid from Staphylococcus epidermidis infected grafts in a mouse model significantly inhibits fibroblast proliferation (60-98% at 7 and 28 days), compared with perigraft fluid from sterile grafts. The fibroblast inhibitor was trypsin-heat resistant and dependent primarily upon the bacteria, not the host proinflammatory mediators or the vascular graft biomaterial. We tested the inhibitory properties of S. epidermidis strains RP62A (slime producer) and RP62NA (nonslime producer) and Staphylococcus aureus strain 502a, using an in vitro tritiated thymidine murine fibroblast (ATCC CCL-12) proliferation assay. Whole killed bacteria, disrupted bacteria (live and killed), bacterial supernatants, and purified cell wall products (peptidoglycan, teichoic acid, and lipoteichoic acid from disrupted bacteria) were studied. Significant fibroblast inhibition occurred for all three bacterial strains with disrupted bacteria (live or killed) and cell free bacteria derived supernatants. The fibroblast inhibitor from disrupted slime producing S. epidermidis was trypsin-heat resistant. The fibroblast inhibitor from disrupted S. aureus and supernatants for all three bacterial strains at 1 x 10(7) were trypsin-heat sensitive. Fibroblast inhibition was not dependent upon bacterial viability and not mediated by bacterial cell wall products. In conclusion, components of slime and nonslime producing S. epidermidis and S. aureus inhibit fibroblast proliferation.
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PMID:Bacterial components inhibit fibroblast proliferation in vitro. 1066 13

We purified and characterized a lectin from the corn coleoptyle (Zea mays). The lectin (CCL) was purified by affinity chromatography on a Lactosyl-Sepharose 4B column. It is a glycoprotein of 88.7 kDa, composed mainly by glutamic, aspartic, glycine, and Ser residues; in a minor proportion, it contained methionine and cysteine residues. Carbohydrates that constituted 12% of the total weight comprised galactose, mannose, and N-acetyl-D-glucosamine. The lectin contained the blocked amino-terminus. Analysis of the lectin, determined from peptides obtained after trypsin digestion by MALDI-TOF (matrix-assisted laser desorption ionization-time of flight), indicated that CCL has 18% homology with a putative calcium-dependent Ser/Thr protein kinase, from Arabidopsis thaliana, and 39% homology with a NADPH-dependent reductase from Z. mays. The lectin showed hemagglutinating activity toward several erythrocytes, including human A, B, and O. Hapten inhibition assays indicated that the lectin interacts specifically with the OH on C4 from galactose residues. OH- on C1 plays a relevant role in the interaction with CCL, since beta-galactose residues are better recognized than those from the anomeric alpha-galactose. Lack of lectin activity was observed in corn extracts; the highest specific activity was obtained from coleoptyle obtained at the 7th day after seeding.
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PMID:Purification and characterization of a galactose-specific lectin from corn (Zea mays) coleoptile. 1173 Oct 83

Concerns over cell line identities and contamination have led investigators to acquire fresh stocks of HeLa CCL-2 cells, but results with the HeLa CCL-2 cells do not always reproduce results with HeLa cells that have long history in the laboratory. When used for TCID(50) assays of Coxsackievirus B3/28 (CVB3/28), HeLa CCL-2 cells returned titers for CVB3/28 that were more than ten-fold lower than titers obtained using laboratory HeLa cells. The viral cytopathic effect was less distinct in the HeLa CCL-2 cultures, suggestive of a mixed population of cells with varied susceptibility to viral cytopathic effect. Analysis of short tandem repeat markers confirmed the identities of the cell lines as HeLa. Subpopulations in the HeLa CCL-2 culture, separated easily based on the speed with which they were released by trypsin-EDTA, differed in their susceptibilities to CVB3/28 cytopathic effect, and in their expression of the Coxsackievirus and adenovirus receptor (CAR). The distinctions between Lab HeLa and HeLa CCL-2 cells were less obvious when infected with CVB3/RD, a strain selected for growth in RD cells. Results that differ among laboratories may be due to the use of HeLa cell strains with different histories, and experiments using HeLa CCL-2 available from the American Type Culture Collection are probably incapable of reproducing many of the published studies of Coxsackievirus that have used HeLa cells with laboratory-dependent histories.
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PMID:HeLa cell heterogeneity and coxsackievirus B3 cytopathic effect: implications for inter-laboratory reproducibility of results. 2340 55

Cryptococcosis, caused by the basidiomycete Cryptococcus neoformans, is a life-threatening disease affecting approximately one million people per year worldwide. Infection can occur when C. neoformans cells are inhaled by immunocompromised people. In order to establish infection, the yeast must bypass recognition and clearance by immune cells guarding the tissue. Using in vitro infections, we characterized the role of mast cells (MCs) in cryptococcosis. We found that MCs recognize C. neoformans and release inflammatory mediators such as tryptase and cytokines. From the latter group MCs released mainly CCL-2/MCP-1, a strong chemoattractant for monocytic cells. We demonstrated that supernatants of infected MCs recruit monocytes but not neutrophils. During infection with C. neoformans, MCs have a limited ability to kill the yeast depending on the serotype. C. neoformans, in turn, modulates the lifespan of MCs both, by presence of its polysaccharide capsule and by secreting soluble modulators. Taken together, MCs might have important contributions to fungal clearance during early stages of cryptocococis where these cells regulate recruitment of monocytes to mucosal tissues.
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PMID:Cryptococcus neoformans Induces MCP-1 Release and Delays the Death of Human Mast Cells. 3145 52


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