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 novel DNA-binding activity, hereafter referred to as MECA, is induced upon transformation of rat embryo fibroblasts by the collaborative action of the oncogenes myc and ras. MECA is targeted to the enhancer "core" element of the Moloney Murine Leukemia Virus LTR. Its binding site can direct transcription from a heterologous promoter and EJras, but not c-myc, potentiates the transcriptional activity. A two point mutation within the enhancer "core" abolishes both DNA-binding by MECA and transcriptional activity. MECA may mediate some of the transforming effects of ras, and thus belongs in the family of transformation-specific DNA-binding activities with members such as AP-1, PEA3 and NF-kB.
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PMID:An enhancer "core" DNA-binding and transcriptional activity is induced upon transformation of rat embryo fibroblasts. 158 May 45

A T cell line from mononuclear cells in the synovial fluid of a patient with polyarthritis was established. The T cell line reacted with serum samples positive for antibodies to human T cell lymphotropic virus type I (HTLV-I) and with monoclonal antibody to HTLV-I p19. In Southern blotting with an env-pX-LTR HTLV-I probe and digestion of T cell line DNA with the restriction enzymes ClaI, DraI, and PstI generated fragments that were identical to those found in two HTLV-I infected T cell lines established from adult T cell leukaemia or HTLV-I associated myelopathy. The T cell line expressed CD2, CD3, CD4, CD45RA, CD29, HLA-DR, CD25, and CD26 antigens, but not CD8 and CD20 antigens. Large amounts of interleukin 6, interferon gamma, and tumour necrosis factor alpha were secreted in the culture supernatants of this cell line. This line helped immunoglobulin production by B cells, but not K562, Raji, and synovial cell lysis.
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PMID:HTLV-I associated arthritis: characteristics of an HTLV-I virus infected T cell line from synovial fluid. 161 38

A region of the human T-cell leukemia virus long terminal repeat (HTLV-I LTR) located between -155 and -117 is important in the regulation of gene expression by the ets family of transcription factors. In an attempt to identify additional cellular transcription factors that bind to this portion of the HTLV-I LTR, we used lambda gt11 expression cloning with oligonucleotides corresponding to this element. A 1239-bp cDNA was isolated from a Jurkat cDNA library, which encoded a protein capable of binding to this purine-rich region. This protein, which we designated human T-cell leukemia virus enhancer factor (HTLF), contains a domain with homology to the recently described fork head DNA binding domain. Chromosome mapping of the HTLF gene demonstrated that it was localized to human chromosome 2p16-p22. HTLF is a unique cellular gene that may function in the transcriptional regulation of HTLV-I LTR.
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PMID:Characterization and chromosomal mapping of the gene encoding the cellular DNA binding protein HTLF. 163 93

Recombination in a bovine papillomavirus shuttle vector carrying direct repeats of Moloney murine leukemia virus LTR sequence was examined. Differently from similar vectors carrying direct repeats of SV40 polyA addition signal or neomycin resistance gene, the vector exhibited no homologous recombination between the repeats. Instead, illegitimate recombination took place. There were two major types of recombination products from the restriction cleavage pattern. The plasmids in independent cellular clones belonging to the same recombination type shared the identical crossover point. Thus, in this plasmid, illegitimate recombination occurred at preferential sites involving exactly the same sequences.
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PMID:Illegitimate recombination in a bovine papillomavirus shuttle vector: a high level of site specificity. 165 50

The polymerase-chain reaction was applied for detection of provirus DNA of the bovine leukaemia virus (BLV). A short fragment of 292 bp including region R and U5 LTR 5' of BLV was amplified, and the optimum parameters of amplification of this fragment were established. Electrophoresis revealed the presence of the 292 bp fragment from the leucocytes of four out of six cows showing a positive serological response to BLV antigens. Application of the polymerase-chain reaction in diagnosis of bovine leukaemia is suggested.
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PMID:Detection of the bovine leukaemia virus by the polymerase chain reaction. 166 66

A human T-cell line producing human T-cell leukemia virus type I (HTLV-I), MT-2, was injected intravenously into female F344 rats aged 5 weeks to make HTLV-I carrier rats. Antibody against HTLV-I was detected at the 5th week after MT-2 injection, and its titer reached a high plateau which continued from the 15th to the 27th week. The antibodies were against p19, p24, p28 and p53 of HTLV-I antigens from MT-2 cells. The gag, pX and LTR nucleotide sequences of HTLV-I provirus were demonstrated by using polymerase chain reaction (PCR) in the peripheral-blood mononuclear cells of 3 rats at the 44th week and 2 at the 66th to 68th week out of 8 F344 rats injected with MT-2 cells. Quantification of the HTLV-I proviral sequence revealed that 30 to 60 molecules were present in 10(5) peripheral-blood mononuclear cells, indicating that the rats were chronically infected with HTLV-I. HTLV-I-infected rats could serve as a small-animal model for studying the pathophysiological state of HTLV-I carriers and also that of HTLV-I infection on various HTLV-I-related diseases, including adult T-cell leukemia and HTLV-I-associated myelopathy.
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PMID:Infection of rats with HTLV-1: a small-animal model for HTLV-1 carriers. 168 81

Southern blot analysis revealed no difference between the DNA from radiation-induced thymic lymphomas and DNA from normal NFS mice. The probes used in the Southern blot analyses used a murine leukemia virus (MuLV) env DNA probe (pXenv), which specifically hybridizes with xenotropic and recombinant viral env genes, and mouse mammary tumor virus (MMTV) DNA probes (MMTV gag-pol, MMTV env, and MMTV LTR). This suggests that radiation leukemogenesis was not associated with gross alteration of the organization of these retroviral genomes. In DNA from radiation-induced thymic lymphoma, there was no indication of gross rearrangement in the common integration site of MuLV, pim-1, or in the common integration sites of MMTV, int-1 and int-2. Dot blot analysis of RNA from radiation-induced thymic lymphomas and normal thymuses demonstrated that there was no substantial difference between them in the expression of retroviral sequences, pim-1, pvt-1, int-1, or int-2, although transcripts that could be hybridized to the retroviral sequences were slightly elevated in some radiation-induced thymic lymphomas. These results show that radiation leukemogenesis does not appear to involve the activation of endogenous type-C and type-B retroviruses.
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PMID:Lack of evidence for the involvement of type-C and type-B retroviruses in radiation leukemogenesis of NFS mice. 169 Apr 35

Activating mutations within the various RAS protooncogenes have been detected in many human and murine hematopoietic neoplasms. Their causal significance has been difficult to assess, partly due to the lack of an animal model directly linking these mutations to hematopoietic neoplasms. A high-titer, helper-free recombinant retrovirus was used to introduce an activated Harvey RAS gene under the transcriptional control of the Moloney leukemia virus LTR into murine bone marrow cells. Eleven of fifteen mice reconstituted with these bone marrow cells developed fatal thymic lymphomas 10-12 week post-transplant. Analysis of DNA and RNA from tumor cells revealed the integrated proviral genome and provirally encoded RAS mRNA respectively. Immunophenotyping and T-cell receptor rearrangement analysis of fresh tumor cells and of cell lines derived from these tumors showed them to be T-cells arrested midway through thymic development. Despite evidence of proviral integration in marrow cells of mice with thymic tumors, no other hematologic abnormalities were detected. The short latency and reproducibility of thymic lymphoma development in mice transplanted with marrow transduced with this retrovirus suggests a direct causal effect of expression of an activated RAS gene in the transformation of a bone-marrow-derived lymphoid progenitor.
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PMID:Introduction of an activated RAS oncogene into murine bone marrow lymphoid progenitors via retroviral gene transfer results in thymic lymphomas. 170 19

The core of retroviruses contains a highly conserved, low molecular weight, basic protein that binds nucleic acids and is essential for genomic RNA packaging. The 56 amino acid protein, NCp10, of Moloney Murine Leukaemia virus (MoMuLV) has the CysX2 CysX4 HisX4 Cys zinc finger-like motif shared by all retrovirus nucleocapsid proteins. The native protein and five modified peptides containing the zinc binding domain were synthesized by solid phase in order to investigate the structural and biochemical role of Zn2+ chelation in MoMuLV NCp10 activity. The purity of the synthetic molecules was verified by HPLC and their sequences were confirmed by amino acid analysis and sequencing in the case of NCp10. Thiol dosage agreed with the theoretical value of free cysteine for all these molecules. Fluorescence measurements performed on synthetic NCp10 and zinc finger fragments showed that the tryptophan quantum yield was Zn2(+)-dependent, allowing a 1:1 stoichiometry for the complex to be determined. The apparent affinity constant of NCp10 for the metal was estimated to be superior to 10(6) M-1. The synthetic protein, in the presence of Zn2+ ions, possesses all the biological properties of NCp10 isolated from virions. It catalyzes both the MoMuLV RNA dimerization and the annealing of the replication primer tRNA(Pro) onto MoMuLV RNA.
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PMID:Solid phase synthesis of the retroviral nucleocapsid protein NCp10 of Moloney murine leukaemia virus and related "zinc-fingers" in free SH forms. Influence of zinc chelation on structural and biochemical properties. 170 45

The herpes simplex virus (HSV) immediate-early protein ICP27 has been postulated to play an auxillary role in HSV. gene expression, augmenting or inhibiting the activation of different viral promoters by the other immediate-early proteins ICPO and ICP4. Here we show that ICP27 alone can up-regulate gene expression of a retroviral vector containing Moloney murine leukemia virus (MoMuLV) regulatory sequences. This is the first report of an effect of ICP27 on gene expression driven by heterologous virus regulatory sequences. The effect does not involve the region of ICP27 which inhibits gene activation of HSV early gene promoters by ICPO and ICP4, but rather is dependent on the same region of ICP27 as is required to augment the activation of HSV late gene promoters by ICPO and ICP4. This indicates that the two activation effects are likely to operate via the same mechanism. Activation by ICP27 is dependent on the 3' LTR and adjacent region of MoMuLV but is independent of the promoter in the 5' LTR which can be replaced by a heterologous promoter such as that of SV40 without affecting activation by ICP27. The significance of this effect for an understanding of the mechanism of action of ICP27 and its role in regulating the gene expression of HSV and potentially of other viruses is discussed.
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PMID:Promoter-independent activation of heterologous virus gene expression by the herpes simplex virus immediate-early protein ICP27. 173 2


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