Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The 71,000 dalton glycoprotein (gp71) purified from Rauscher murine leukemia virus (R-MuLV) by affinity chromatography specifically binds to murine but not other mammalian cells in culture. Binding is prevented by specific antiserum raides to gp71 (anti-gp71). The binding assay as described in this report can detect receptors on as few as 300 murine cells, and with 1 X 10(5) cells gives significant binding with 30 sec. The results show that the purified glycoprotein retians biologic activity and can form a stable complex with specific receptors on mouse cell membranes. The assay can therefore be used to characterize the nature of the cellular receptors that are essential for leukemia virus infection. Purified gp71 binding to mouse cells is prevented if the cells are actively producing related ecotropic type C viruses, presumably because the receptors are occupied and are not available to bind exogenously applied gp71. The binding of gp71 to murine cells is enhanced by the presence of calcium ions and low pH. Binding studies performed using an excess of 125I-gp71 indicate the NIH/3T3 cells bind approximately 5.3 X 10(5) molecules of 125I-gp71 per cell.
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PMID:Membrane receptors for murine leukemia viruses: characterization using the purified viral envelope glycoprotein, gp71. 0 13

Expression of Gix surface antigen on thymocytes is an inherited mendelian train of certain strains of mice. We report here the following new findings: (a) Gix antigen was found free in the serum of Gix+ mouse strains. (b) Expression vs. nonexpression of Gix antigen was invariably correlated with presence or absence of the group-specific antigen of Murine leukemia virus (MuLV) gp69/71 in the serum of mice of inbred and segregating populations. (c) Gix antigen could be removed from normal Gix+ mouse serum by precipitation with antiserum to MuLV gp 69/71. (d) Anti-gp69/71 serum was weakly cytotoxic for Gix+ thymocytes, and partially blocked the cytotoxic activity of Gix antibody for Gix+ thymocytes. (e) Purified AKR virus absorbed Gix activity, and disruption of the virions did not increase their absorbing capacity. These serological data indicate that Gix antigen is a constituent of gp69/71, the glycoprotein which is the major component of the MuLV envelope. On present evidence, Gix antigen is represented in intact virions and is probably accessible to Gix antibody.
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PMID:Relation of GIX antigen of thymocytes to envelope glycoprotein of murine leukemia virus. 4 10

The 70,000 molecular weight glycoprotein (gp70) of a type-C RNA virus originally isolated from a woolly monkey has been partially purified and immunologically characterized. Evidence that this viral protein is viral coded was derived from studies showing its antigenic properties to be unaltered by virus passage in cells of different species. A broadly reactive competition immunoassay was developed utilizing antiserum prepared against feline leukemia virus to precipitate 125I-labeled woolly monkey virus gp70. Gibbon and woolly viruses, as well as feline and several mouse type-C viruses, all reacted with equal efficiency in this assay. In contrast, an endogenous virus of the baboon failed to cross-react, suggesting that viruses of this latter group are less immunologically related to the others. In a homologous competition immunoassay for the woolly viral glycoprotein, the woolly virus was readily distingusihed from otherwise colsely related viruses of gibbon apes. These findings demonstrate the pronounced type-specific antigenic dterminants possessed by this viral protein. The antigenic determinants of gp70 responsible for neutralization have also been investigated.
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PMID:Antigenic determinants of the 70,000 molecular weight glycoprotein of woolly monkey type C RNA virus. 5 82

Leukemic cells from all human chronic granulocytic leukemia (CGL) and some acute myelomonocytic leukemia (AMML) donors are lysed by rabbit antisera to a purified glycoprotein of Friend murine leukemia virus (FLV gp71) in a microcytotoxicity assay. These antisera are not cytotoxic to cells from patients with acute myelocytic leukemia (AML), acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), or to peripheral blood lymphocytes from normal donors. A goat antiserum to gradient purified FLV in addition to reacting with cells from CGL and AMML donors also reacted with cells from AML patients and some ALL donors. However, this antiserum failed to react with cells from CLL patients. Peripheral blood and bone marrow leukocytes prepared from leukemic patients in clinical remission failed to react with antisera to FLV and FLV gp71. Absorption experiments demonstrated that the antigen on CGL cells which is reacting with the antiserum to FLV gp71 is also present on normal human platelets and neutrophils. Similar absorption studies showed that the antigen on AML cells detected by the FLV antiserum is not present on normal leukocytes and platelets and appears to be related to the major internal p30 antigens of mammalian RNA tumor viruses. Another antigenic relationship between oncornaviruses and membrane antigens of human leukemia cells was shown by the ability of FLV antigens to absorb the cytotoxic reactivity of nonhuman primate antisera detecting human leukemia-associated antigens. FLV and FLV gp71 antigens were able to absorb all cytotoxic activity of monkey and chimpanzee antisera to human myeloid leukemia antigens when these antisera were tested with CGL cells. These two approaches to an analysis of cross-reactivity indicate that the antigenic determinant(s) detected by the cytotoxic reactions of the FLV gp71 antiserum with human CGL cells is different from the determinant on FLV gp71 which is responsible for the inhibition of the reactivity of simian antisera with CGL cells. Since the goat and rabbit antisera to FLV and FLV gp71 are able to distinguish AML from CGL cells by direct cytotoxicity testing and absorption, they may be valuable reagents for the serological diagnosis of myeloid leukemia. In addition, since peripheral blood cells from AML and CGL patients in clinical remission were seronegative, the antisera may be valuable as management aids. The data in this report indicates that whatever the mechanism of leukemogenesis is in man, cells from CGL and AML patients possess certain membrane antigens which cross-react with FLV structural components such as p30 and gp71.
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PMID:Relationships between membrane antigens of human leukemic cells and oncogenic RNA virus structural components. 5 69

The humoral immune response against endogenous ecotropic murine leukemia viruses (MuLV) was examined in irradiated and control C57BL/6 mice. Control mice developed antibodies against MuLV slowly throughout life. In contrast, within 2-3 mo after irradiation 90% of irradiated C57BL/6 mice had developed detectable antibodies against MuLV. The characteristics of this immune response, however, were identical in control and irradiated mice in terms of peak titers, specificity for endogenous ecotropic MuLV, and reactivity against the ecotropic viruses' glycoprotein (gp71). Moreover, the rate of appearance of antibodies against MuLV in irradiated mice and the peak titers were generally not affected by age at irradiation, dose of irradiation (two, three, or four treatments of 175 R), or bone marrow reconstitution. Although the ability of irradiation to accelerate the appearance of antibody in a population of C57BL/6 mice suggested activation of endogenous ecotropic MuLV, there was no apparent correlation between the appearance of this immune response or its persistence and the development of lymphoma. Thus, the incidence of lymphoma was comparable in mice that: (a) developed no immune response; (b) developed an immune response only transiently after irradiation; or (c) developed an immune response which persisted until death from lymphoma. Moreover, experimental conditions that alter the ability of irradiation to induce leukemia, such as age, dose, or bone marrow reconstitution did so without significantly altering either the rate of appearance of a humoral immune response to MuLV or its peak titers. The results, therefore, fail to demonstrate any seroepidemological relationship between endogenous ecotropic MuLV and radiation-induced leukemia.
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PMID:Radiation leukemia in C57BL/6 mice. I. Lack of serological evidence for the role of endogenous ecotropic viruses in pathogenesis. 6 28

The specificity of a single rabbit antiserum pool raised against the purified major glycoprotein, gp71, of Friend murine leukemia virus was determined for a variety of virus-producing mouse, feline, and gibbon ape cell lines by viable cell membrane immunofluorescence absorption. Among murine cells examined, Friend gp71 type specificity was shared only with Rauscher virus-producing cells, and a group specificity was present for all the murine leukemia virus-producing cells tested. Friend and Rauscher murine leukemia virus-infected cells shared interspecies cross-reactivity with feline leukemia and gibbon ape lymphoma virus-producing cells. However, Moloney, Gross, and other virus-producing murine cells shared some, but not all, of these gp71 interspecies determinants with the feline and primate cells. Immunoferritin electron microscopy localized these gp71 antigenic determinants on both virus and cell membranes.
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PMID:Immunofluorescent analysis of expression of the RNA tumor virus major glycoprotein, gp71, on surfaces of virus-producing murine and other mammalian species cell lines. 6 19

The expression of the major glycoprotein, gp71, of murine leukemia virus was studied on the surfaces of a variety of normal murine cell lines with a monospecific rabbit antiserum raised against purified Friend murine leukemia virus gp71. Using viable cell membrane immunofluorescence, most established and early passage normal murine cell lines were significantly reactive with the antiserum, irrespective of neoplastic transformation, strain genotype, or whether they were of embryonic or adult tissue origin. The only murine cells tested not detectably expressing gp71 determinants were BALB/3T3 lines. Although some Friend gp71 interspecies reactivity was discernible on normal murine cells, the principal reactivity was shown to be group specific. Fresh thymocytes from BALB/cJ (GIX-), C57BL/6J (GIX-), and 129/J (GIX+) mouse strains were also reactive with Friend gp71 antiserum, and this activity, as well as that of an antiserum prepared against purified AKR gp71, were also group specific. An activity discriminating GIX+ from GIX- thymocytes was not observed with either Friend or AKR gp71 antisera.
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PMID:Immunofluorescent analysis of expression of the RNA tumor virus major glycoprotein, gp71, on the surfaces of normal murine cells. 6 20

Using the Ouchterlony immunodiffusion method and indirect immunofluorescence tests on tissue slices the antigenic structure of iAp of mouse mammary tumour origin has further been investigated. Antisera against iAp, MTV-B particles, B particle polypeptide p27 and glycoprotein gp52, and leukemia C-type particles were used in these studies. The most prominent antigen of iAp in mammary tumours was found to be identical to the p27 antigen of B particles. This finding was not unexpected in view of recently published data by other authors showing the presence of p27 in iAp of leukemia cells and Leydig cell tumours. The p27 polypeptide is considered to be a group-specific antigen of mouse mammary tumour viruses associated with iAp of different tissue sources and inner structural components of mature B particles. On the other hand, the gp52 antigen and leukemia virus antigens were shown to be absent from iAp of mammary carcinomas. Therefore, the assumption is confirmed that the gp52 glycoprotein represents a group-specific antigen of B type viruses, presumably located at the virion surface. The failure to demonstrate leukemia virus antigens in iAp supports the suggestion that this kind of particles is not related to C type viruses.
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PMID:Presence of the p27 antigenicity and absence of the gp52 antigenicity and leukemia virus antigens in intracytoplasmic A particles (iAp) of mouse mammary tumour origin. 6 45

A new retravirus (SMRV) isolated from a squirrel monkey, Saimiri sciureus, has an Mg2+-dependen reverse transcriptase and a buoyant density of 1.17 g/cm3 in sucrose and 1.21 g/cm3 in cesium chloride, similar to the mouse mammary tumor virus and the Mason-Pfizer monkey virus. The polypeptide patter of SMRV as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis was distinct from the reported polypeptide patterns of known retraviruses. Four major polypeptides of molecular weights 40,000, 20,000, 14,000 and 8,000 were resolved in virus propagated in human, mink, and canine cells. In A204 human rhabdomyosarcoma cells, a protein of 73,000 daltons (gp73) represented the major viral glycoprotein as determined by [3H]glucosamine labeling. Additional proteins were also observed, but their presence depended on the cell type in which the virus was propagated. In both species-and interspecies-specific assays, no antigenic relatedness was observed between SMRV and Mason-Pfizer monkey virus, mouse mammary tumor virus, baboon endogenous virus (BaLV), woolly monkey virus (SSV-1), murine leukemia virus, endogenous feline type C virus (RD-114), bovine leukemia virus, and equine infectious anemia virus. These findings indicate that SMRV represents a new retravirus and the first isolate from a New World monkey.
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PMID:Characterization of a retravirus isolated from squirrel monkeys. 6 28

Cell membranes of Moloney lymphoma cells (YAC, of strain A origin) were solubilized by NP40. The antigenicity of the solubilized protein fraction was assayed by inhibition of the corresponding cytotoxic reaction against YAC target cells. The Moloney leukemia virus (MLV)-determined cell surface antigen (MCSA) was detected with mouse antisera, produced by the repeated inoculation of heavily irradiated YAC cells into syngeneic mice. Virion proteins gp71, p30, p15, p12 and p10 were identified with goat or rabbit antisera against purified Rauscher and Friend leukemia virus proteins. MCSA was found to bind to Con-A--Sepharose and was eluted by mannoside together with H-2A AND GP71. In contrast, p30, p12, p10 and part of p15 and p15(E), were not retained on the column and could be separated from MCSA. Passage of the glycoprotein fraction through Sephadex G-200 led to the separation of MCSA activity from gp71 and H-2A. MCSA eluted between the immunoglobulin (IgG) and the bovine serum albumin (BSA) size markers. MCSA could be also separated from the known viral proteins and from H-2 by velocity centrifugation in sucrose gradients. It sedimented with approximately 6.6 S ahead of gp71 (4.4 S) and H-2 (3.2 S). It is suggested that MCSA may be a glycoprotein with an approximate molecular weight of 110,000 and distinct from the known viral proteins gp71, p30, p15(E), p12, p10 and from H-2.
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PMID:Separation of the Moloney leukemia virus-determined cell surface antigen (MCSA) from known virion proteins associated with the cell membrane. 7 Dec 77


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