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)

A previously described 120,000 dalton polyprotein, P120, encoded by the Abelson strain of murine leukemia virus (AbLV) is compared to translational products representing the entire Moloney murine leukemia virus (MuLV) genome. Each of three [35S]-methionine tryptic present in Moloney-MuLV Pr65gag are also represented in Pr180gag-pol. Of these, one peptide corresponding to Moloney-MuLV p12, but neither of two p30 specific peptides are present in AbLV P120. None of the twelve remaining methionine containing peptides present in AbLV P120 appear to correspond to those of either Moloney-MuLV Pr82env. AbLV P120 and a 110,000 dalton polyprotein encoded by a second transforming isolate of mouse origin, designated AK-T8, are both shown to be highly phosphorylated. Sites of phosphorylation included known phosphorylated structural (p12) components, as well as components encoded by acquired cellular sequences. Immunoprecipitates of AbLV P120 obtained from either cells or pseudotype virions are shown to contain protein kinase activity which recognizes AbLv P120 as substrate. This activity may represent an intrinsic property of the polyprotein itself or represent a cellular enzyme associated with AbLV P120 in the form of an enzyme-substrate complex.
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PMID:Abelson murine leukemia virus: characterization of a polyprotein containing phosphorylated component(s) encoded by newly acquired sequences. 625 63

A glycoprotein of molecular weight 130,000 (gP130) has been precipitated from the cytoplasm of GR-strain mouse mammary tumor (GR-MMT) cells by a rabbit antiserum (anti-MMTV) to GR-strain mouse mammary tumor virus (GR-MMTV). This protein was not precipitated by antisera specific for detergent-disrupted C3H-strain MMTV (C3H-MMTV); C3H-MMTV glycoproteins; C3H-MMTV nonglycosylated proteins; GR-MMTV p25 or p12; RIII strain (milk) MMTV proteins; or Rauscher murine leukemia virus (R-MuLV) proteins; nor was it precipitated by normal rabbit serum. Two-dimensional thin layer analysis of 35S-methionine-containing tryptic peptides revealed that five of nine gp33 peptides and one of seven gp55 peptides are shared by gP130 and gPr76env. The envelope protein precursor, gPr76env, contains all of the gp33 peptides and six of seven gp55 peptides. One peptide in gPr76env, possibly a gp55-gp33 junction peptide, is also apparently present in gP130. Six of ten p25 peptides and four more gag-related peptides are shared by PR78gag and gP130. Protein gP130 also contains several tryptic peptides not found in gPr76env or in the core protein precursors Pr78gag, Pr110gag or Pr180gag-pol. Radioimmunoprecipitation experiments showed that gP130 could be precipitated from extracts of GR-MMTV cells with anti-MMTV serum even after antibodies to the known MMTV structural proteins had been removed from the serum by absorption. Both gP130 and a second protein, p30, were found in immunoprecipitates of detergent-disrupted isotopically labeled GR-MMTV treated with the absorbed anti-MMTV serum. These results suggest that antibodies to gP130 in the anti-MMTV serum are capable of recognizing those protein sequences unique to gP130; that is, those protein sequences which are not related to viral structural proteins. In light of these data and data published previously, gP130 is apparently a polyprotein containing juxtaposed components translated from the 5' and 3' end of the MMTV genome and protein components not previously identified as virus-specific.
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PMID:A unique glycoprotein containing GR-mouse mammary tumor virus peptides and additional peptides unrelated to viral structural proteins. 625 70

Mink cells nonproductively-infected with the weakly-transforming T-8 isolate of murine leukemia virus (MuLV) express a 110,000 mol wt polyprotein designated T-8 P110. By immunoprecipitation analysis, T-8 P110 is shown to contain AKR-MuLV amino terminal gag gene-specific components (p15, p12) but to lack p30, p10, gp70, and p15(E) antigenic determinants. These observations are further substantiated by tryptic peptide analysis indicating T-8 P110 to share approximately six lysine-containing tryptic peptides with AKR-MuLV Pr65gag, and none with AKr-MuLV Pr82env. Furthermore, of seven methionine-containing T-8 P110 tryptic peptides, at least four can be conclusively shown not to be present in either AKr-MuLV Pr180gag/pol or Pr82env. A clonal mink cell line nonproductively infected by T-8, and expressing high levels of P110, although not morphologically transformed, is shown to lack elevated levels of tyrosine-specific protein kinase activity and reduction of epidermal growth factor binding sites characteristic of cells transformed by many other RNA-transforming viruses. These findings argue either that the T-8 viral genome contains acquired cellular sequences encoding a portion of P110, or that T-8 P110 represents an inphase deletion of AKR-MuLV Pr180gag/pol with extensive posttranlational modification and that an as yet unidentified protein is responsible for T-8 associated transformation.
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PMID:Identification of tryptic peptides unique to a 110,000-molecular weight polyprotein encoded by the T-8 isolate of murine leukemia virus. 625 65

Antiserum to the p15(E) polypeptide of Rauscher murine leukaemia virus (R-MuLV) precipitated two proteins from purified virions of feline leukaemia virus (FeLV) with apparent mol. wt. of 18500 and 155000 on SDS-polyacrylamide gels. These proteins have been designated p15(E) and p12(E), in line with the nomenclature for MuLV proteins. Like the analogous protein of MuLV, FeLV p15(E) was found to be disulphide-linked to the virion glycoprotein, gp70. FeLV p15(E) was sensitive to digestion of intact virus particles with the proteolytic enzyme, bromelain, indicating that this protein is on the outer surface of the virion. An analysis of cat sera for precipitating activity for FeLV p12(E) showed this only in sera from cats which had recovered from FeLV infection and had virus-neutralizing activity.
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PMID:Polypeptides of feline leukaemia virus: identification of p15(E) and p12(E). 625 28

Murine fibroblasts transformed by transfection with DNA from mink cells infected with the Snyder-Theilen strain of feline sarcoma virus and subgroup B feline leukemia virus were analyzed for the presence of integrated proviral DNA and the expression of feline leukemia virus- and feline sarcoma virus-specific proteins. The transformed murine cells harbored at least one intact feline sarcoma virus provirus, but did not contain feline leukemia virus provirus. The transformed murine cells expressed an 85,000-dalton protein that was precipitated by antisera directed against feline leukemia virus p12, p15, and p30 proteins. No feline oncornavirus-associated cell membrane antigen reactivity was detected on the surfaces of the transformed murine cells by indirect membrane immunofluorescence techniques. The 85,000-dalton feline sarcoma virus-specific protein was also found in feline cells transformed by transfection. However, these cells also contained env gene products. The results of this study demonstrate that the feline sarcoma virus genome is sufficient to transform murine cells and that expression of the 85,000-dalton gag-x protein is associated with transformation of both murine and feline cells transformed by transfection.
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PMID:Biochemical characterization of cells transformed via transfection by feline sarcoma virus proviral DNA. 626 44

Tissue distribution of radiation leukemia virus (RadLV) was examined after its inoculation into normal C57BL/6J (B6) mice, B6 mice bearing a transplantable, non-virus-producing thymic lymphoma (RL12-NP), and B6 mice bearing a transplanted non-virus producing, Harvey murine sarcoma virus-transformed fibrosarcoma. Virus expression was determined by competition radioimmunoassay for murine leukemia virus (MuLV) p30 (predominant group-reactive antigen of MuLV) and for RadLV p12 (a highly type-specific MuLV polypeptide) and by membrane immunofluorescence for cell surface gp71 (predominant envelope glycoprotein of MuLV). Normal adult B6 mice were given three sequential iv injections of RadLV and were examined several times up to 200 days later for the appearance of neoplastic disease or expression of virion antigens. No clinical abnormalities were noted, and animals remained healthy for greater than 200 days. Significant levels of MuLV p30 and RadLV p12 were detected only in the thymuses. Organs and tumors from RL12-NP-inoculated animals contained low or nondetectable levels of virion antigens. Inoculation of mice with RL12-Rad, a cell line derived by in vitro infection of RL12-NP cells with RadLV, produced widespread, discrete metastatic tumors and infiltrated the lymphoid organs of B6 mice in a pattern identical to that observed after administration of RL12-NP cells. Lymphoid organs of RL12-Rad-inoculated animals expressed variable levels of virion antigens reflecting differences in the extent of tumor cell infiltration as opposed to virus spread from tumor to host cells. Administration of infectious RadLV systemically into RL12-NP tumor-bearing animals converted these tumors to viron antigen expressors with levels in superinfected tumors equivalent to those found in RL12-Rad-induced tumors. Infection was highly selective, and host tissues were minimally contaminated by the inoculated virus. Part of this selectivity was explained by the thymotropic property of RadLV. A rapidly dividing murine fibrosarcoma was not infected by RadLV, but this same non-virus-expressing tumor could be infected by common fibrotropic MuLV isolates.
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PMID:In vivo antigenic modification of tumor cells. III. Metastatic thymic lymphoma specifically infected by thymotropic retrovirus. 626 78

Recombinant viruses were generated in tissue culture between Rauscher murine leukemia virus (MuLV) temperature-sensitive (ts) mutants restricted at different steps in virus replication and a mouse endogenous xenotropic virus, BALB:virus-2. Mutants used included ts 28, a late mutant which releases noninfectious viruses at 39 degrees C, and ts 29, a double mutant with a ts lesion in its reverse transcriptase and a late block affecting virus budding. Immunological typing of the translational products of clonal recombinant viruses made it possible to establish their partial genetic maps and localize regions of the viral genome affected by different ts lesions. Recombinants involving Rauscher MuLV ts 28 invariably contained BALB-virus-2 p15, p12, and p30 proteins, localizing the late defect in replication by this mutant to the 5' moiety of the viral gag gene. All ts 29-derived recombinants contained the entire BALB:virus-2 gag and pol genes. Substitution of the pol gene is in agreement with the reported thermolability of Rauscher MuLV ts 29 reverse transcriptase (Tronick et al., J. Virol. 16:1476-1482, 1975). Substitution of the gag gene suggests that internal structural proteins are actively involved in the virus budding processing. Rauscher MuLV recombinants were used to establish the genetic map of the Rauscher MuLV genome by T1 oligonucleotide fingerprinting analysis. Detection of Rauscher MuLV T1 oligonucleotides in representative recombinant viruses, whose protein phenotypes were established by immunological techniques, permitted their assignment to specific regions of the viral genome. The genetic map of Rauscher MuLV generated in these studies should be useful for identifying and characterizing the viral gene(s) involved in leukemogenesis.
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PMID:Recombinants between temperature-sensitive mutants of rauscher murine leukemia virus and BALB:virus-2: genetic mapping of the Rauscher murine leukemia virus genome. 626 12

A cell line (LB59Ly) derived from the leukocytes of a leukaemic cow was established as a monolayer, which spontaneously released large amounts of a retrovirus. This virus was found to be indistinguishable from the bovine leukaemia virus (BLV) produced by the commonly used high-producing heterologous cell line (FLK-BLV). Like the latter, its reverse transcriptase activity was greater in the presence of Mg2+ cations than in the presence of Mn2+ cations; its polyacrylamide gel electrophoresis pattern showed the presence of gp51, p24, p15, p12 and p10, and the antigenicity of the two major proteins completely cross-reacted with those of BLV from FLK-BLV cells. The virus was infectious and induced early and late polykaryocytosis, the specificity of which was demonstrated by use of specific anti-BLV sera.
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PMID:Establishment and propagation of a bovine leukaemia virus-producing cell line derived from the leukocyte of a leukaemic cow. 627 Feb 54

IgG and circulating IgG immune complexes (CIC) were purified from plasma of three pet cats persistently infected with feline leukemia virus (FeLV) by adsorption to, and elution from, Staphylococcus aureus Cowan I. CIC were then separated from free IgG by sucrose gradient ultracentrifugation and were analyzed for the presence of FeLV structural proteins and corresponding specific antibodies. Radioimmunoprecipitation analysis indicated that FeLV envelope (gp70) and major core (p30) proteins, along with cat IgG heavy and light chains, were present in the CIC from all three cats. Further analysis of the CIC from one of the cats also revealed the presence of FeLV core proteins p15 and p12. IgG purified from isolated CIC was also shown to bind specifically to purified FeLV gp70, p30, and p15. These data provide direct evidence for FeLV-specific CIC in the plasma of persistently viremic pet cats, and suggest these animals are immunologically response to the virus even though free antibodies against the major structural proteins cannot be demonstrated in standard assays.
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PMID:Isolation and characterization of circulating feline leukemia virus-immune complexes from plasma of persistently infected pet cats removed by ex vivo immunosorption. 628 36

Cultured human hematopoietic cells from several normal and leukemic sources, including those cells initiated after exposure to primate type C retroviruses were tested for their capacity to induce tumors in young athymic BALB/c (nu/nu) mice after sc inoculation. An attempt was made to correlate these results with virus expression and chromosome patterns. Progressively growing tumor formation was observed in 5 of 18 normal diploid B-lymphoblast lines from normal peripheral blood and in one of three diploid B-lymphoblast lines from leukemic donors established after infection with primate type C viruses (gibbon ape leukemia virus or simian sarcoma virus). In contrast, none of eight spontaneously transformed B-lymphoblast lines with normal diploid karyotypes formed progressively growing tumors, although one formed a tumor that remained the same size (0.5 cm) for several months. Progressive tumor formation occurred in four of seven previously established cell lines of different cell types that had abnormal karyotypes. Of the normal diploid B-lymphoblast cultures exposed to type C viruses, 12 were tested for the presence of viral RNA and structural proteins (p12, p30, gp70), and this information was correlated with tumorigenicity. Four of the six cultures expressing viral RNA or proteins were tumorigenic, whereas only one of six cultures that did not express virus information was positive. The results of this study suggest that expression of type C viral RNA and proteins by human B-lymphoblasts increases their tumorigenicity in nude mice. It is also apparent that caution must be used in attempts to correlate cell tumorigenicity and chromosome abnormalities in nude mice.
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PMID:Effect of type C viral expression and cellular karyotype on human B-lymphoblast tumorigenicity in nude mice. 628 77


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