Disease relevance of Mlv1

• However, rearrangements were detected in Abelson murine leukemia virus-transformed bone marrow cells and in spontaneous thymic lymphomas from C.B-17scid mice [1].
• We placed the SV40 early region within this DNA and after transfection of cells producing helper Moloney murine leukemia virus, SV40 retroviruses (MV40) could be rescued [2].
• In some instances, mouse cells infected by M-MuLV reveal additional proviruses beyond those seen in the uninfected cell [3].
• DNAs from three different M-MuLV-induced thymomas indicate, as in rat cells, multiple possible integration sites [3].
• Cloning revealed a retroviral insert 0.7-1.3 kb 5' to c-myc in two T lymphomas induced by Soule murine leukemia virus and in a spontaneous T lymphoma ( Tikaut ) of an AKR mouse, a strain in which leukemogenesis involves recombinant retroviruses (MCF viruses) [4].

Psychiatry related information on Mlv1

• 334C murine leukemia virus, which induces a high incidence of lymphatic leukemias (80-90%) in susceptible mice following a long latency period, was found to cause a severe in vivo suppression of direct plaque-forming cells from the spleen, following antigenic stimulation with sheep red blood cells [5].
• Permissiveness to Moloney Murine Leukemia Virus (MoMuLV) expression was examined during preimplantation and early postimplantation development of the mouse embryo [6].
• Because platelet-activating factor (PAF) has been implicated in the pathogenesis of HIV-associated dementia complex, brain PAF levels were measured in LP-BM5 MuLV-infected mice [7].
• Because 129/J mice are susceptible to experimental SLE and to infection with the BM5def murine leukemia virus (MuLV) mixture but do not develop the lymphoproliferative/ immunodeficiency disorder known as murine AIDS (MAIDS), we superimposed this infection on immunization with the 16/6 Id [8].
• Since learning and memory performance deficits can be related to attention deficits, we assessed the effect of LP-BM5 MuLV infection on sustained attention performance using a two-choice serial reaction time task [9].

High impact information on Mlv1

• Reverse transcriptase of Moloney murine leukemia virus binds to eukaryotic release factor 1 to modulate suppression of translational termination [10].
• Predisposition to lymphomagenesis in pim-1 transgenic mice: cooperation with c-myc and N-myc in murine leukemia virus-induced tumors [11].
• Transgenic mice bearing the pim-1 gene supplemented with an upstream immunoglobulin enhancer and a downstream murine leukemia virus long terminal repeat express pim-1 mRNA at high levels in both B and T cells [11].
• Using oligonucleotide probes specific for different classes of murine leukemia virus, we have identified and cloned a provirus present in HRS/J hr/hr animals but absent in HRS/J +/+ [12].
• Abelson murine leukemia virus-transformed precursor B lymphocytes from scid (severe combined immunodeficient) mice, like A-MuLV transformants from normal mice, actively rearrange segments of their Ig heavy chain variable region gene locus during growth in culture [13].

Chemical compound and disease context of Mlv1

• Stimulation with bacterial lipopolysaccharide (LPS) of splenic B-lymphocytes infected in vitro with Friend virus complex increased the number of cells with replicating murine leukemia virus (MuLV) [i.e., infectious centers (IC)] up to 100-fold [14].
• Hydroxyurea (HU), given ip four times, each time at 500 mg/kg in 6-hour intervals, was used to treat DBA/2 mice with Friend murine leukemia virus-induced polycythemia (F-MuLV-P) [15].
• Ethidium bromide significantly inhibited the in vivo growth of transplanted adenovirus 12-induced tumor cells of CBA mice, simian virus 40-induced tumor cells of hamsters, and murine leukemia virus-induced lymphoma cells of BALB/c mice [16].
• Detection of a recombinant murine leukemia virus-related glycoprotein on virus-negative thymoma cells [17].
• Moloney murine leukemia virus-derived retrovirus vectors that contain human factor IX cDNA linked to heterologous promoters and the neomycin-resistant gene were constructed and employed to prepare recombinant retroviruses [18].

Biological context of Mlv1

• The integrated genome of murine leukemia virus [3].
• Data from back-crosses of the F1 hybrid to each parent and from BALB/c x B6 recombinant inbred strains indicate that the phenotype of enhanced MuLV production results from interaction of two unlinked loci, dominant (+/+) alleles of which are carried by either parent [19].
• Identification of mouse chromosomes required for murine leukemia virus replication [20].
• The mouse c-abl gene, part of the sequence of which was captured in Moloney murine leukemia virus to generate the transforming gene (v-abl) of the Abelson murine leukemia virus, has been isolated and characterized [21].
• These results suggest that integration of M-MuLV at the Mov13 locus leads to insertion mutagenesis, resulting in embryonic arrest between day 12 and day 13 of gestation [22].

Anatomical context of Mlv1

• Murine leukemia virus-induced T-cell lymphomagenesis: integration of proviruses in a distinct chromosomal region [23].
• Two different kappa RNA species, one the same size as the MPC-11 kappa fragment RNA, frequently are present in kappa RNA-containing Abelson murine leukemia virus-transformed lymphoid cells as well as in 18 and 19 day murine fetal liver [24].
• The mode of action of interferon in de novo Moloney murine leukemia virus (Mo-MuLV) infection of mouse bone marrow/thymus (TB) cells was studied [25].
• Immunocytochemical detection of a murine leukemia virus-related nuclear antigen in mouse oocytes and early embryos [26].
• Two different pathogenic effects of the Friend ecotropic murine leukemia virus (F-MuLV) were distinguished by serial examinations of hematocrits and reticulocyte counts of IRW mice inoculated as newborns [27].

Associations of Mlv1 with chemical compounds

• Although 5-azacytidine decreased the level of DNA methylation, it did not activate M-MuLV in undifferentiated cells [28].
• Ultrastructural evidence of abundant type C viruses within beta cells of treated mice suggests that streptozotocin may activate murine leukemia virus in vivo in susceptible hosts [29].
• Relation of GIX antigen of thymocytes to envelope glycoprotein of murine leukemia virus [30].
• Thymocytes of several mouse strains were tested for expression of the gp69/71 envelope component of murine leukemia virus by surface iodination, followed by immunoprecipitation and sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis [31].
• Inhibition of in vitro Friend murine leukemia virus infection of lipopolysaccharide-activated B-cells with concanavalin A [14].

Physical interactions of Mlv1

• A versatile and potentially general approach to the targeting of specific cell types by retroviruses: application to the infection of human cells by means of major histocompatibility complex class I and class II antigens by mouse ecotropic murine leukemia virus-derived viruses [32].
• Footprints on the viral DNA ends in moloney murine leukemia virus preintegration complexes reflect a specific association with integrase [33].
• Ubiquitin is covalently attached to the p6Gag proteins of human immunodeficiency virus type 1 and simian immunodeficiency virus and to the p12Gag protein of Moloney murine leukemia virus [34].
• A mutant Moloney murine leukemia virus was created in which the binding site for the embryonal long terminal repeat binding protein had been replaced with a synthetic linker sequence [35].
• Amphotropic murine leukemia virus is preferentially attached to cholesterol-rich microdomains after binding to mouse fibroblasts [36].

Regulatory relationships of Mlv1

• Characterization of pal-1, a common proviral insertion site in murine leukemia virus-induced lymphomas of c-myc and Pim-1 transgenic mice [37].
• Activation of multiple genes by provirus integration in the Mlvi-4 locus in T-cell lymphomas induced by Moloney murine leukemia virus [38].
• Stability of AML1 (core) site enhancer mutations in T lymphomas induced by attenuated SL3-3 murine leukemia virus mutants [39].
• In these studies, we show that infection of cells by M-MuLV activates expression of Rel family transcription factors [40].
• We report a new common proviral insertion site in murine leukemia virus-induced T cell lymphomas to be N-myc [41].

Other interactions of Mlv1

• Mice that carry both Inc-1 and Inb-1 yield 10- to 50-fold more virus-producing cells than parental strains on induction with halogenated pyrimidines in vitro and demonstrate enhanced murine leukemia virus production in vivo [42].
• We found that the second intron of Stat5a was one of the common integration sites of the endogenous ecotropic murine leukemia virus, i.e., SL/Kh virus integration-1 (Svi1), in early pre-B lymphomas in SL/Kh mice [43].
• c-myb is a frequent target of retroviral insertional mutagenesis in murine leukemia virus-induced myeloid leukemia [44].
• Mlvi-1 defines a genetic locus representing a common domain for proviral DNA integration in Moloney murine leukemia virus-induced rat thymic lymphomas [45].
• In vitro DNA binding assays, using prokaryotically expressed ALF1 proteins, demonstrated specific binding of the ALF1 proteins to the Akv murine leukemia virus E-box motif ACAGATGG [46].

Analytical, diagnostic and therapeutic context of Mlv1

• In radioimmunoassays, it cross-reacts completely with RadLV/VL3, a virus obtained from RadLV-induced C57BL/Ka thymic lymphoma cells in culture, and slightly with a xenotropic virus (BALB:virus-2) and with AKR MuLV [47].
• Relationship of infectious murine leukemia virus and virus-related antigens in genetic crosses between AKR and the Fv-1 compatible strain C57L [48].
• These viruses from tumor cell cultures were excellent sources of MuMTV 3H-complementary DNA (complexed to 60-70S RNA) and radioactive 60-70S RNA, sufficiently free of contaminating murine leukemia virus nucleic acids, that can be used in molecular hybridization experiments [49].
• Expression of the ecotropic virus was, therefore, transient, as assayed by immunofluorescence, XC syncytia formation, and virus isolation from MuLV gsa-positive thymus cells [50].
• After cocultivation with Balb/3T3 cells chronically infected with a murine leukemia virus (MuLV), a focus-forming principle that transformed 3T3 cells, secondary BALB/c mouse embryo and WAG/Rij rat embryo fibroblasts were rescued [51].

References