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:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As part of an inquiry into factors that determine the virulence of fixed rabies virus, mouse neuroblastoma cells were infected in culture with high virulence and low virulence strains of Flury HEP virus. Low virulence virus infection differed from high virulence virus infection in (1) its more rapid production of progeny virus in the early cycles of virus infection as shown by the number of extracellular virus particles and the infectivity of the supernatant fluid; (2) its earlier development of viral antigens on the cell surface; and (3) its earlier and more severe morphologic alteration of the cell surface. Where applicable, the differences were corroborated by scanning and transmission electron microscopy of the infected cells using the critical point drying technique on whole cells. The number of cells susceptible to complement-dependent immunolysis was almost proportional to the number of cells that were surface antigen-positive regardless of the strain of the virus used. Implications of the difference in the kinetics of virus production and of the development of surface antigens between low and high virulence strains are discussed.
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PMID:Rabies virus infection in mouse neuroblastoma cells. 6 72

A new cell line derived from a woodchuck hepatitis surface antigen-positive woodchuck hepatocellular carcinoma has been established and named T3-HEP-W1. This new cell line was established directly from a primary woodchuck hepatocellular carcinoma. Adaptation of the cells to the in vitro culture condition was completed after 3 months, with the doubling time of 24 hr. The morphologic features of the cell by light microscopy were of an epithelial type. The modal chromosome number was 100. Ornithine and tyrosine aminotransferase activities were detected. Production of albumin was negative. Integration of woodchuck hepatitis virus DNA was demonstrated by Southern blot analysis, although the secretion of woodchuck hepatitis surface antigen was not detected. T3-HEP-W1 is quite different from the previously reported WH257GE10 cell line and provides another in vitro model for the study of human hepatocellular carcinoma related to hepatitis B virus.
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PMID:Establishment of a new cell line from a woodchuck hepatocellular carcinoma. 333 96

The human hepatoma cell line, PLC/PRF/5, which is persistently infected with hepatitis B virus (HBV), has integrated HBV-DNA, secretes HBV surface antigen (HBsAg), and does not grow readily in congenitally athymic (nu/nu) mice. The present investigation was undertaken to ascertain whether the low tumorigenicity of this cell line was governed by a host immune response and/or was related to expression of HBsAg. Subcutaneous injection of 4-5 X 10(6) cells into BALB/c nude mice produced localized encapsulated tumors with morphologic features of primary hepatocellular carcinoma in 25% of the animals within 29-40 d. No tumor growth was observed at lower cell inocula. In contrast, SK-HEP-1, an HBV-negative human hepatoma cell line, produced tumors at 1-5 X 10(6) cells inocula in 66% of the animals. Immunosuppression of mice with antilymphocyte serum (ALS) or irradiation increased tumor incidence in mice inoculated with 1 X 10(6) PLC/PRF/5 cells to almost 100% and produced local invasiveness. Immunosuppression also reduced the latency, i.e., time to tumor appearance, and increased mean tumor weight. These results suggest that tumorigenicity was limited by the host immune response. The nature of the response was delineated by treating nude mice challenged with tumor cells with sheep anti-mouse interferon globulin (anti-IFN). When 2 X 10(6) cells were injected, tumor growth occurred in 75% of anti-IFN-treated mice, whereas controls injected with the same number of cells, but not receiving anti-IFN, failed to develop tumors. The tumors in the anti-IFN-treated mice were highly invasive and the latency period until tumor appearance was reduced to 3-5 d. An inverse correlation was found between susceptibility of the hepatoma cells to natural killer (NK) activity in vitro and resistance to tumor growth in vivo. In vitro cytotoxicity for PLC/PRF/5 cells was eliminated by anti-NK 1.1 and complement, establishing the effector cell as an NK cell. NK cell activity 14 d after inoculation of mice with PLC/PRF/5 cells was augmented against PLC/PRF/5 target cells but not against SK-HEP-1 cells. Treatment of mice with ALS, irradiation, or anti-IFN abolished NK activity against PLC/PRF/5 cells. Co-cultivation of nude mouse spleen cells with PLC/PRF/5 but not with HBsAg or SK-HEP-1 cells induced secretion of murine IFNalpha. These results suggest that the IFN/NK cell system may play a role in limiting tumorigenicity and invasiveness of HBV-infected human hepatocellular carcinoma cells by a mechanism similar to that found for other cells persistently infected with viruses.
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PMID:Role in nude mice of interferon and natural killer cells in inhibiting the tumorigenicity of human hepatocellular carcinoma cells infected with hepatitis B virus. 619 49

Temperature-sensitive (ts) mutants of the rhabdoviruses vesicular stomatitis virus and Chandipura virus have been used to measure the appearance of virus antigen on the surface of infected cells by the technique of surface analysis by bacterial adherence and scanning electron microscopy (SABA/SEM). The number of staphylococci specifically adhering to antiserum-treated infected PTK-2 or BSC-1 cells at permissive (31 degrees C) and restrictive (39 degrees C) temperatures was followed in time-course experiments and a close correspondence was observed between the proportion of staphylococci bound at 39 degrees C and the known phenotypic properties of the ts mutants. Virus surface antigen was undetected in cells infected by transcription- and replication-defective ts mutants with thermolabile L proteins under restrictive conditions up to an input multiplicity of infection of 50, and in cells infected by a replication-defective NS protein mutant. Some surface antigen was detected late in infection in PTK-2 cells infected by a replication-defective N protein mutant. Surface antigen accumulated normally in maturation-defective mutants with lesions in envelope proteins. These results establish the suitability of the SABA/SEM technique for quantitative estimation of virus antigen on the surface of infected cells.
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PMID:Measurement of surface antigen by specific bacterial adherence and scanning electron microscopy (SABA/SEM) in cells infected by vesiculovirus ts mutants. 627 72

During 1961-75, 128 cases of primary liver carcinoma (PLC) in the Radiation Effects Research Foundation life-span study extended sample and 301 cases of liver cirrhosis in the pathology study sample were observed. The presence of hepatitis B surface antigen (HBsAg) was assessed in all of the cases with the use of orcein and aldehyde fuchsin stains and was confirmed by the immunofluorescence technique. The incidence of PLC was two times higher in Nagasaki than in Hiroshima, which was statistically significant, but little difference was noted in the prevalence of cirrhosis in the two cities. Findings that might possibly explain the higher PLC incidence in Nagasaki were 1) the 2.3 times higher presence in Nagasaki than in Hiroshima of HBsAg in the livers of subjects without liver disease and 2) the two times higher prevalence in Nagasaki than in Hiroshima of cirrhosis with PLC. We believe that the higher incidence of PLC in Nagasaki is attributable to hepatitis B virus infection, although other factors (e.g., immunologic competence affected by radiation) cannot be excluded. In both cities, a suggestive relationship of radiation dose to cirrhosis prevalence, but not to PCL prevalence, was noted. To clarify possible radiation effects on cirrhosis prevalence, further follow-up of the populations of these two cities is necessary.
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PMID:Primary liver carcinoma and liver cirrhosis in atomic bomb survivors, Hiroshima and Nagasaki, 1961-75, with special reference to hepatitis B surface antigen. 675 25

Aflatoxin B1 (AFB1) has been postulated to be a hepatocarcinogen in humans, possibly by causing p53 mutations at codon 249. AFB1 is metabolized via the phase I and II detoxification pathways; hence, genetic variation at those loci may predict susceptibility to the effects of AFB1. To test this hypothesis, genetic variation in two AFB1 detoxification genes, epoxide hydrolase (EPHX) and glutathione S-transferase M1 (GSTM1), was contrasted with the presence of serum AFB1-albumin adducts, the presence of hepatocellular carcinoma (HCC), and with p53 codon 249 mutations. Mutant alleles at both loci were significantly overrepresented in individuals with serum AFB1-albumin adducts in a cross-sectional study. Mutant alleles of EPHX were significantly overrepresented in persons with HCC, also in a case-control study. The relationship of EPHX to HCC varied by hepatitis B surface antigen status and indicated that a synergistic effect may exist. p53 codon 249 mutations were observed only among HCC patients with one or both high-risk genotypes. These results indicate that individuals with mutant genotypes at EPHX and GSTM1 may be at greater risk of developing AFB1 adducts, p53 mutations, and HCC when exposed to AFB1. Hepatitis B carriers with the high-risk genotypes may be an even greater risk than carriers with low-risk genotypes. These findings support the existence of genetic susceptibility in humans to the environmental carcinogen AFB1 and indicate that there is a synergistic increase in risk of HCC with the combination of hepatitis B virus infection and susceptible genotype.
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PMID:Susceptibility to hepatocellular carcinoma is associated with genetic variation in the enzymatic detoxification of aflatoxin B1. 789 76

Bone marrow (BM) stromal cells express CD10 (cALLA), a surface antigen now known to be a neutral endopeptidase (NEP-24.11). The function of CD10 in BM stroma is unknown, although purified NEP-24.11 is known to degrade different substrates including interleukin 1 beta (IL-1 beta). We have therefore employed a CD10-positive BM stromal cell line (L2AK) which proliferates in response to IL-1 beta to test the hypothesis that degradation of this cytokine is one of the functions of stromal CD10. We first showed that [3H]thymidine incorporation by L2AK cells is enhanced by IL-1 beta in a clear dose-dependent manner. Addition of the CD10 inhibitor, phosphoramidon, together with IL-1 beta resulted in a left shift in the dose-response curve which corresponded to a 10-fold potentiation of the IL-1 beta effect. These results indicate that CD10 on bone marrow stromal cells can degrade IL-1 beta and therefore provide a local control of the effects of this, and possibly other, growth factor(s).
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PMID:A function of CD10 on bone marrow stroma. 799 15

A cell monolayer radioimmunoassay was established to detect hepatitis B virus (HBV)-binding activity. HBV was shown to bind to HepG2 and HuH7 cells, but not to LTK- and HeLa cells. The binding activity was inhibited by peptide 21-47 from the large hepatitis B surface antigen (L-HBsAg) region, but not by other peptides from the L- and middle-HBsAg. A monoclonal antibody to L-HBsAg (MA18/7) and a polyclonal antibody to HBsAg (anti-HBs) also inhibited the binding. However, only the Fab fragment of MA18/7 showed blocking activity, suggesting that these two antibodies may neutralize virus by different mechanisms. Excess HBV was able to saturate the binding activity of HepG2 cells. The virus was also shown to be internalized; virus DNA was detected in the cytoplasmic fraction 1-2 hr postadsorption and was associated with the nuclear fraction 2 hr later. Furthermore, immunoprecipitation experiments showed that the virus DNA remained encapsidated 48 hr after internalization. Nuclear fractionation experiments showed that the encapsidated HBV DNA remained associated with the nuclear membrane. Trypsinization of intact nuclei resulted in disassociation of the nucleocapsid from the nuclear membranes, suggesting that the nuclear membrane presents a barrier to intact HBV virions or nucleocapsids. This may explain why HepG2 cells are refractile to infection although permissive for HBV replication after transfection of viral DNA.
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PMID:Adsorption and penetration of hepatitis B virus in a nonpermissive cell line. 818 45

The retinal pigment epithelium (RPE) differs from other epithelia in that the apical surface is not free; instead, it interacts with both photoreceptors and a specialized extracellular material, the interphotoreceptor matrix. Biochemical characterization of the apical and basolateral surfaces of RPE in adult rat eye cups, using a novel in situ biotinylation assay, revealed very different protein compositions and identified a major surface antigen, RET-PE2, with a predominantly apical distribution (approximately 74%). The apical polarity of RET-PE2 was confirmed by immunofluorescence and laser scanning confocal microscopy. In striking contrast, RET-PE2 antigen was preferentially basolateral in primary cultures derived from adult rat RPE and in an immortalized RPE cell line (RPE-J). Under all conditions, RET-PE2 was highly soluble in Triton X-100 (> 81% at 4 degrees C), suggesting that its redistribution was not dependent on changes in cytoskeletal interactions. Analysis of the localization of RET-PE2 in normal rats at postnatal (PN) days 1, 7, and 14 indicated that RET-PE2 redistributes from predominantly basolateral to predominantly apical during that time. Since photoreceptors develop during the first two weeks after birth in the rat, our results suggest that the apical redistribution of RET-PE2 is dependent on the establishment of adult interactions between the RPE and the neural retina and/or the interphotoreceptor matrix, either via direct contacts or through alterations in the intracellular sorting patterns of RPE cells.
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PMID:The polarity of the plasma membrane protein RET-PE2 in retinal pigment epithelium is developmentally regulated. 900 37

Osteoclast development from hematopoietic bone marrow precursors is associated with the expression of various enzymes, receptors, adhesion molecules, and other specialized components. Among these is a novel 150 kD superoxide dismutase-related membrane glycoprotein, originally identified by its reaction with the anti-osteoclast monoclonal antibody 121F. This antigen is uniquely restricted to osteoclasts in bone, universally present on osteoclasts from multiple species, induced during osteoclast differentiation in vitro and in ovo, and required at high levels for avian osteoclastic bone pit resorption. Expression of a comparable human antigen was investigated using human leukemic FLG 29.1 cells capable of differentiating towards an osteoclast-like phenotype. Phorbol ester, 1,25 (OH)2 vitamin D3, and osteoblast-derived soluble factors elicited dose and time-dependent inductions of this antigen as measured by enzyme-linked immunosorbent assay (ELISA) and immunocytochemical staining, coincident with their display of multiple other osteoclastic features. Synergistic interactions of these modulators led to further elevations in the ultimate expression levels of this antigen, although not to the full extent associated with in vivo-formed avian osteoclasts. The potent antiresorptive hormone 17beta-estradiol, but not its inactive alpha isomer, partially suppressed the phorbol ester-induced elevation of the 121F antibody-reactive antigen in FLG 29.1 cells as it does in avian osteoclast-like cells. Characterization of the human antigen isolated from FLG 29.1 cells by 121F immunoaffinity purification demonstrated that this regulated membrane component was synthesized by these human cells, more abundant following their differentiation into osteoclast-like cells, and similar biochemically and immunologically to the 150 kD integral membrane glycoprotein previously described from avian osteoclasts. Therefore, this report is the first documentation that human osteoclast-like FLG 29.1 cells express, in a developmentally regulated fashion, a homolog of the specific 150 kD avian osteoclast surface antigen that is related to superoxide dismutase, a protective free radical scavenging enzyme and is essential for osteoclastic bone resorption.
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PMID:A human homolog of the 150 kD avian osteoclast membrane antigen related to superoxide dismutase and essential for bone resorption is induced by developmental agents and opposed by estrogen in FLG 29.1 cells. 905 69


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