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)

Antisera produced in mice recognize primarily type-specific antigenic determinants on both the major core protein, p30, and the major envelope proteins, gp70 and p15(E), of the endogenous leukemia viruses (MuLV) of BALB/c mice. Three different mouse sera were investigated in detail. (i) Antisera prepared in C57BL/6 mice against the AKR leukemia K36 reacted with the gp70, p15(E), and p30 proteins of MuLV. Certain pools of the C57BL/6 anti-AKR K36 serum contained antibodies which serologically distinguished the p30 proteins of N-ecotropic, B-ecotropic, and xenotropic BALB/c MuLV. (ii) Antisera prepared in BALB/c mice against the BALB/c sarcoma 1315 contained antibodies that reacted with a type-specific antigen of the 1315 MuLV gp70 that is not found on other BALB/c MuLV. (iii) The normal sera of multiparous BALB/c mice contained antibodies that reacted with gp70 and p15(E) proteins of ecotropic MuLV. Sera from some of these mice contained antibodies that serologically distinguished the gp70 of N-ecotropic and B-ecotropic BALB/c viruses. These results emphasize the utility of mouse antisera in the serological typing of MuLV. Furthermore, the antigenic differences observed in the p30 and gp70 proteins should be of particular use in the future analysis of recombinant BALB/c MuLV.
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PMID:Detection of polymorphism in BALB/c leukemia viruses with mouse antisera. 9 60

Oncornaviruses, which contain a virion-associated protein kinase, were found to possess phosphoproteins as virion structural components. One major phosphoprotein common to strains of laboratory and wild mouse oncornaviruses and a strain of feline leukemia virus was shown to be a polypeptide of about 12, 000 mol wt. In addition to this, the Kirsten strain of murine sarcoma virus contained a second major phosphoprotein of about 10, 000 mol wt, and mouse erythroblastosis virus contained a second major phosphoprotein that was either identical to or comigrated with the virion glycoprotein of about 74, 000 mol wt. The major phosphoprotein of RD-114 virus was found to be of about 16, 000 mol wt. The major phosphoamino acid of the 12, 000-mol wt polypeptide of the mouse erythroblastosis virus was identified as phosphoserine, and that of the 16, 000-mol wt polypeptide of the RD-114 virus was identified as phosphothreonine.
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PMID:Phosphoproteins: structural components of oncornaviruses. 16 71

The protein and glycoprotein composition of Kirsten murine leukaemia-sarcoma virus (KiMSV(KiMuLV) was studied using SDS-polyacrylamide gel electrophoresis. Twenty-three polypeptides and three glycoproteins were detected following electrophoresis by staining with Coomassie blue and PAS or by autoradiography of isotopically labelled virus. Protein components were assigned positions in the virus particle, envelope, nucleoid or intermediate area based on iodination with lactoperoxidase and sedimentation in potassium citrate equilibrium gradients. The KiMSV (KiMuLV) envelope contained 11 polypeptides and three glycoproteins. The virus nucleoid and intermediate area were each composed of six proteins. The protein composition of KiMSV(KiMuLV) was highly reproducible when virus was harvested from cells of the same subcluture generation. However, the protein profiles were altered with repeated in vitro passages of the virus-producing cell line.
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PMID:Proteins of Kirsten murine leukaemia-sarcoma virus: localization within the virus particle by iodination and fractionation techniques. 16 14

A high-titered non-focus-forming virus, FBJ-MuLV (murine leukemia virus), present in FBJ tumor preparations, inhibited significantly the expression and production of FBJ-MuSV (murine sarcoma virus) in tissue culture. This "autoinhibition" was comparable to that observed when a 3- to 4-log excess of infectious MuLV was added to standard MuSV. The degree of inhibition was influenced by the tropism of the MuLV (or the ease of spread and propagation of MuLV in certain cells), multiplicity of infection by MuLV, amount of excess MuLV, and ability of the MuSV-transformed cells to replicate independently. The FBJ MuLV-MuSV complex may be a model system for the detection of sarcoma viruses in spontaneous tumors in various animals where inhibition by excess nontransforming virus could be an important biologic phenomenon.
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PMID:Studies of FBJ osteosarcoma virus in tissue culture. II. Autoinhibition of focus formation. 16 61

This study describes an unusual type of virus seen when a feline leukemia virus (FeLV) pseudotype of murine sarcoma virus (MuSV) obtained by cocentrifugation procedures infected feline embryo cells (FEF) and two Crandell cat cell lines (CrFK1, CrFK2). When all three cell cultures were infected with MuSV-FeLV, only FEF and CrFK2 were transformed and only these showed normal and aberrant virus. The CrFK1 infected with MuSV-FeLV did not transform but did replicate normal type-C virus with a 50-A intermediate coat. The virus replicated in the two transformed lines showed three particles; a normal particle with a 50-A intermediate coat, a normal particle with a 100-A intermediate coat, and an aberrant particle with a 100-A intermediate coat.
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PMID:Aberrant viruses in cells infected with murine sarcoma virus-feline leukemia virus. 16 69

Characterization of ribonucleic acid content of particles released from cultures of marrow cells of leukemic patients indicates the presence of RNA molecules of size and base sequence characteristic of oncornarviruses. Seventeen marrow samples obtained from leukemic patients in relapse or in a chronic phase of the disease yielded particles containing high-molecular-weight RNA with a sedimentation velocity (about 70 S) similar to that obtained for murine oncornavirus RNA. Eight of nine marrow samples from non-leukemic patients did not yield detectable high-molecular weight RNA. Among patients in firm hematological remission, three of three samples from patients with acute lymphoblastic leukemia and three of nine samples from patients with acute myeloblastic leukemia were positive for high-molecular-weight RNA. The base sequence of the RNA in particles was characterized by synthesizing complementary (3-H)DNA in an endogenous reaction and hybridizing to excess RNA from known oncornaviruses. Hybridization of 40-60% of input complementary DNA to simian sarcoma virus RNA was detected. No monology was detected with an avian oncornavirus (Rous sarcoma virus) while an intermediate level of homology (10-30%) was detected in hybridization to murine sarcoma virus (Kirsten) and murine leukemia viruses (Rauscher, Moloney, and Gross).
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PMID:Viral-related information in oncornavirus-lik particles isolated from cultures of marrow cells from leukemic patients in relapse and remission. 16 62

Isolates of a sarcoma (Moloney)-leukemia virus complex prepared as cell-free extracts from mouse tumors showed no enhancement in infectivity by DEAE-D either in the sarcoma moiety measured by focus formation or in the leukemia moiety measured by XC cell assay. The sarcoma moiety was not enhanced by DEAE-D in MEM and modified McCoy's 5a media or when varying amounts of FCS and glutamine were included in the media. Progressive enhancement of viral infectivity by DEAE-D was found when the viral preparations were passaged serially in MEF cells. DEAE-D ALSO ENHANCED TUMOR FORMATION IN VIVO BY TISSUE CULTURE PASSAGED VIRUS.
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PMID:Effect of diethylaminoethyl-dextran on the replication of a murine sarcoma (Moloney)-leukemia virus complex in mouse embryo cultures (38577). 16 73

Non-produces (NP) human cells were isolated from transformed foci induced by the Kirsten mouse sarcoma virus. These morphologically altered NP cells produced neither infectious virus nor complement-fixing antigens of the murine sarcoma-leukemia virus complex. However, the sarcoma virus genome could be rescued from these NF cells by co-cultivation with cells carrying "helper" Kirsten mouse leukemia virus or Woolly Monkey leukemia virus. The possible usefulness of these cells in efforts designed to detect covert or repressed RNA tumor viruses in various animal and human tissues is discussed.
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PMID:Non-producer human cells induced by murine sarcoma virus. 16 48

A horse skin cell line (E. Derm, NBL-6, CCL-57) was susceptible to focus formation by the Kirsten mouse sarcoma virus, feline sarcoma virus (ST stain) and the MSV pseudotypes with woolly monkey, gibbon monkey, RD-114, AT-124, baboon placenta and murine xenotropic (BALB/c 3T3 and C57L/JD) type-C viruses. Foci were detected within 5 days after infection and the transformed cells continued to produce infectious virus and group-specific antigen of their respective type-C leukemia viruses. The transformation efficiency of various type-C sarcoma viruses in horse cells was also very high.
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PMID:Transformation of horse skin cells by type-C sarcoma viruses. 16 52

6-(P-hydroxyphenylazo)-uracil (HPUra) reduced by dithiothreitol inhibited AMV or RLV virion associated exogenous RNA-dependent DNA polymerase reactions. However, the inhibition was variable from experiment to experiment and was not consistent with the base specificity of HPUra seen for inhibition of gram positive DNA-dependent DNA polymerases. Increasing the concentration of dithiothreitol reversed the inhibition. Furthermore, at non-toxic concentrations, HPUra did not influence the plating efficiency of RLV in tissue culture, as measured by the ability to induce foci on sarcoma virus positive-leukemia virus negative cells. Oxidation of dithiothreitol in the presence or absence of HPUra was followed spectrophotometrically under enzyme conditions. HPUra catalyzed the oxidation of dithiothreitol under these conditions. Since dithiothreitol is required for optimum reaction rates, as well as complete disruption of virus in some polymerase assay systems, the oxidation of dithiothreitol in the presence of HPUra is sufficient to explain the inhibition seen.
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PMID:Inhibition of RNA-dependent DNA polymerase reaction by 6-(p-hydroxyphenylazo)-uracil: A result of drug induced dithiothreitol oxidation. 16 20


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