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)

Feline leukemia virus contains a protease which apparently has the same specificity as murine leukemia virus protease. It cleaves in vitro the Pr65gag of Gazdar-mouse sarcoma virus into the constituent p15, p12, p30, and p10 proteins. We purified the protease and determined its NH2-terminal amino acid sequence (the first 15 residues). Alignment of this amino acid sequence with the nucleotide sequence (I. Laprevotte, A. Hampe, C. H. Sherr, and F. Galibert, J. Virol. 50:884-894, 1984) reveals that the protease is a viral-coded enzyme and is located at the 5' end of the pol gene. As previously found for murine leukemia virus (Y. Yoshinaka, I. Katoh, T. D. Copeland, and S. Oroszlan, Proc. Natl. Acad. Sci. U.S.A. 82:1618-1622, 1985), feline leukemia virus protease is synthesized through in-frame suppression of the gag amber termination codon by insertion of a glutamine in the fifth position, and the first four amino acids are derived from the gag gene.
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PMID:Translational readthrough of an amber termination codon during synthesis of feline leukemia virus protease. 299 7

The 24,000-molecular-weight major internal protein (p24) and the 15,000-molecular-weight nucleic acid binding protein (p15) of human T-cell leukemia virus type II (HTLV-II) were subjected to amino acid composition and amino-terminal amino acid sequence analysis. A comparison of amino acid composition of p24 and p15 of HTLV-II with those of the analogous proteins of HTLV-I revealed that these two proteins share overall similarity. Further, alignment of the amino-terminal amino acid sequence for the first 27 residues of p24 and 34 residues of p15 from HTLV-II showed extensive sequence homology with analogous proteins of HTLV-I. These data suggest that although disease associated with HTLV-I is malignant T-cell leukemia and that associated with HTLV-II is a relatively benign variant of hairy-cell leukemia, HTLV-I and HTLV-II are closely related to each other, at least in their gag-gene-encoded sequences.
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PMID:Human T-cell leukemia virus type II: primary structure analysis of the major internal protein, p24 and the nucleic acid binding protein, p15. 299 80

Three distinct monoclonal antibodies (MAbs) specific for human T-cell leukemia virus type-I (HTLV-I) core proteins with molecular weights of 24 kDa (p24), p19 or p15 were produced, characterized and compared. These antibodies were named NOR-1 (anti-p24, IgG2a), GIN-7 (anti-p19, IgG2b) and FR-45 (anti-p15, IgG2a). Immunofluorescence assay showed that they reacted specifically with methanol-fixed cells of virus-bearing cell lines, and that only GIN-7 bound, albeit weakly, to the surface of a small percentage of viable cells. Like natural antibodies to HTLV-I in human serum, GIN-7 stained the fixed cells brightly and diffusely, and gave more intense fluorescence than NOR-1 and FR-45, which stained restricted areas of the cells. NOR-1, GIN-7 and FR-45 specifically precipitated core proteins p24, p19 and p15, respectively, from a lysate of HTLV-IMT-2 labelled with 35S-cysteine. NOR-1 precipitated p53, p36, and p24, GIN-7 precipitated p53, p32, p28 and p19, and FR-45 precipitated p53, p36, and p15 from a lysate of 35S-cysteine-labelled MT-2 cells. GIN-7 also precipitated p32, p28 and p19 from a lysate of MT-2 cells, labelled by surface iodination, but NOR-1 and FR-45 did not detect any proteins in this lysate. GIN-7 also detected p28 in 3H-glucosamine-labelled MT-2 cells. Antibody binding competition assay showed that the sera of ATL patients significantly interfered with the binding of NOR-1 and GIN-7 but not with that of FR-45, to antigens of disrupted virus of MT-2 cells. This complete set of MAbs against the HTLV-I gag gene products is useful for biological and functional studies of the HTLV-I core proteins.
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PMID:Antigens related to three core proteins of HTLV-I (p24, p19 and p15) and their intracellular localizations, as defined by monoclonal antibodies. 300 Sep 53

Extensive fusion occurs upon cocultivation of murine fibroblasts producing ecotropic murine leukemia viruses (MuLVs) with a large variety of murine cell lines in the presence of the polyene antibiotic amphotericin B, the active component of the antifungal agent Fungizone. The resulting polykaryocytes contain nuclei from both infected and uninfected cells, as evidenced by autoradiographic labeling experiments in which one or the other parent cell type was separately labeled with [3H]thymidine and fused with an unlabeled parent. This cell fusion specifically requires the presence of an ecotropic MuLV-producing parent and is not observed for cells producing xenotropic, amphotropic, or dualtropic viruses. Mouse cells infected with nonecotropic viruses retain their sensitivity toward fusion, whereas infection with ecotropic viruses abrogates the fusion of these cells upon cocultivation with other ecotropic MuLV-producing cells. Nonmurine cells lacking the ecotropic gp70 receptor are not fused under similar conditions. Fusion is effectively inhibited by monospecific antisera to gp70, but not by antisera to p15(E), and studies with monoclonal antibodies identify distinct amino- and carboxy-terminal gp70 regions which play a role in the fusion reaction. The enhanced fusion which occurs in the presence of amphotericin B provides a rapid and sensitive assay for the expression of ecotropic MuLVs and should facilitate further mechanistic studies of MuLV-induced fusion of murine cells.
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PMID:Ecotropic murine leukemia virus-induced fusion of murine cells. 300 11

An effective subunit vaccine against feline leukemia virus infection and related diseases has been developed. The source of the vaccine immunogen is feline retrovirus persistently infected cells that continuously synthesize and shed virus polypeptides. Western blot analysis identifies FeLV-gp70, p27, p15, p12, and p10 in the subunit vaccine preparation. Cats immunized with the vaccine developed antibodies to a 70,000 MW protein of the vaccine that seems to be distinct from, but related to the FeLV-gp70 polypeptide.
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PMID:Feline leukemia vaccine: efficacy, contents and probable mechanism. 300 10

The antibody response against the envelope proteins of a variety of cloned highly and poorly oncogenic dualtropic mink cell focus-inducing (MCF) murine leukemia viruses (MuLV) was studied and compared with the antibody response against ecotropic isolates. MCF viruses evoke stronger antibody responses than ecotropic MuLV isolates. Although these MCF viruses are highly polymorphic with respect to their gp70 and p15(E) envelope proteins, generally a similar H-2-linked immune response gene control of anti-viral antibody responses is observed. Neonatally infected BALB/c (H-2d) and C57BL/10 (B10,H-2b) mice are high responders and B10.A (H-2a) mice, congenic at the major histocompatibility complex (H-2) with B10, low responders. No correlation was found between the expression of any single gp70 or p15(E) epitope of the infecting MCF virus and the magnitude of the antibody response. This indicates that the level of the H-2 regulated anti-MuLV envelope antibody response is most likely determined by a MuLV antigen shared by all MuLV isolates examined. The magnitude of the antibody response against highly oncogenic and against poorly oncogenic MCF virus does not differ significantly. The combined data indicate that the intrinsic oncogenic potency encoded by the viral genome is a more important feature of oncogenesis than the level of antiviral envelope antibody response evoked by the MCF virus. However, the oncogenic properties of a single murine leukemia virus may vary among H-2 congenic mice, correlated with their H-2-dependent capacity to produce antiviral antibodies.
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PMID:Differences in oncogenicity among murine leukemia virus isolates are not correlated with the magnitude of H-2 regulated anti-viral envelope antibody responses. 302 Mar 21

The organization of the transforming protein encoded by Abelson murine leukemia virus (A-MuLV) in transformed lymphoid and fibroblast cells was examined using immunofluorescent analysis. Antibodies specific for v-abl were capable of detecting cytoplasmic Abelson protein molecules in fixed cells, but none were able to stain the surface of live A-MuLV transformed cells. However, a series of monoclonal antibodies selected for the ability to bind to the surface of A-MuLV-transformed cells did stain live cells. These antibodies were shown to react with a determinant within the helper virus-derived p15 sequences that are present at the amino terminus of the Abelson protein, indicating that gag-derived determinants are exposed on the surface of transformed cells. The inability of a p12-specific monoclonal antibody to stain live cells indicates that only a small portion of the amino terminal sequences are exposed. Examination of the ability of these antibodies to react with Abelson protein encoded by a series of gag deletion mutants suggests that the determinant recognized by these antibodies lies between amino acids 38 and 114 of p15.
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PMID:Gag-derived but not abl-derived determinants are exposed on the surface of Abelson virus-transformed cells. 302 Jul 82

The proteolytic processing of the gag precursor polypeptide pr65gag of simian sarcoma-associated virus (SSAV) has been studied in vivo and in vitro. In SSAV-infected cells (i.e., in vivo) proteins of 52 and 38 kDa and the viral protein p30 could be immunoprecipitated with anti-p30 serum. This cleavage pattern is only in part imitated by in vitro cleavage of the isolated pr65gag with avian myeloblastosis virus (AMV) protease p15. However, in vitro incubation of isolated pr65gag with detergent-disrupted SSAV particles generated products identical in size to those found in vivo, i.e., proteins of 52 and 38 kDa and p30. The extent of cleavage is dependent on the concentration of the disrupted virions added to the incubation mixture. Studies with protease inhibitors suggest that the SSAV enzyme is a serine-type protease like that of other mammalian retroviruses and unlike the protease of avian viruses. The SSAV protease activity eluted from a molecular sieve column in a range of about 10-15 kDa reflecting the molecular weight of the murine leukemia virus (MuLV) protease (Mr = 13.5K). Thus, it appears that there is a close similarity between the proteolytic enzymes present in different mammalian retroviruses such as MuLV and SSAV.
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PMID:Characterization of a virus-specific proteolytic activity processing the gag precursor of the simian sarcoma-associated virus. 302 76

The murine leukemia virus envelope protein is synthesized as a precursor molecule, Pr85env, which is proteolytically cleaved at an arginine residue to produce two mature envelope proteins, gp70 and p15(E). The results presented here indicate that mutation to lysine of the arginine found at the envelope precursor cleavage site results in a precursor which is cleaved with an efficiency at least 10-fold lower than the efficiency with which the wild-type protein is cleaved. This mutation has been used to investigate the requirement for envelope protein processing in various aspects of retroviral infection. Viruses produced by cells transfected with mutant proviral clones are approximately 10-fold less infectious than wild-type viruses. Mutant viruses are incapable of inducing XC cell syncytium formation and are 100-fold less efficient than wild-type viruses at rendering cells resistant to superinfection. Envelope glycoproteins bearing the lysine mutation are found in reduced amounts on the surface of infected cells, and as a result mutant virions contain significantly less envelope protein than do wild-type virions. The phenotypic effects of the processing mutation described here are most likely the result of this paucity of envelope glycoproteins in virions carrying the mutation.
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PMID:The role of envelope glycoprotein processing in murine leukemia virus infection. 303 73

The translocation t(11;20)(p15;q11) was found as the sole acquired clonal chromosome abnormality in two patients with acute myeloid leukemia. The bone marrow morphology in both cases corresponded to the M2 subtype of the French-American-British (FAB) classification. None of the patients achieved complete remission, and both died less than 6 months after diagnosis. This particular translocation has not previously been reported in acute nonlymphocytic leukemia.
Leukemia 1988 Jul
PMID:A new specific chromosomal rearrangement, t(11;20)(p15;q11), in myeloblastic leukemia with maturation. 316


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