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)

We introduced an LTR-driven mouse c-myc second and third exon, Tn5Neo gene construct into the inducible human leukemia line HL60 using an amphotropic retroviral vector system. Over 90% of the cells became neo-resistant and the transfected myc gene was transcribed in several neomycin resistant clones. Making use of the simultaneous presence of the different myc genes in the same cell, we compared expression of the corresponding mRNAs after differentiation and their decay mechanisms.
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PMID:Efficient retroviral transfer of a mouse c-myc construct into HL60. 267 38

Human T-cell leukemia virus type I (HTLV-I) is the etiological agent of adult T-cell leukemia. The 3' end of HTLV-I proviral DNA encodes the synthesis of two regulatory proteins, tax and rex. The 40-kDa tax protein is a nuclear protein which positively stimulates transcription from the U3 region of the viral long terminal repeat sequence. Three 21-base pair sequences in the U3 region have been found to serve as the cis-element for tax-mediated trans-activation. We now report that the tax protein can trans-activate HTLV-I LTR in the absence of de novo cellular protein synthesis. Saturated mutagenesis of the 21-base pair repeat sequence showed that specific mutations clustered in sequences homologous to the cAMP responsive element (TGACGTCA) abolish trans-activation by tax. Furthermore, although the TGACGTCN element is nearly palindromic, the mutations that abolish trans-activation are localized exclusively in the 5' 6 bases, suggesting the orientation of this element may play a role in transcription. That the purified tax protein does not bind the 21-base pair repeats or nonspecific DNA lends further support to the notion that tax protein does not directly interact with the 21-base pair repeats to activate transcription. Instead, tax most likely acts via cellular transcriptional factor(s) to bring about trans-activation.
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PMID:HTLV-I tax gene product activates transcription via pre-existing cellular factors and cAMP responsive element. 276 59

We analyzed embryonal carcinoma cell lines infected with a recombinant Moloney murine leukemia virus. Lines that carried but did not express the neo gene retained a provirus of LTR-gag-pol-neo-LTR, where LTR is a long terminal repeat, whereas all G418-resistant lines deleted regions that included the primer binding site and the splicing donor site. This suggested the presence of multiple inhibitory elements.
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PMID:Deletions in a recombinant retrovirus genome associated with its expression in embryonal carcinoma cells. 277 84

The transactivator protein tax of the human T-cell leukemia virus type I, HTLV-I, is responsible for transactivation of gene expression of viral and cellular genes and is involved in the onset of adult T-cell leukemia, ATL. Genetic deletion studies have implicated a region of the HTLV-I LTR designated as tax-acceptor region, TAR, which is the target of the tax protein. Using antibodies against a tax carboxyterminal synthetic decapeptide the tax protein was purified from an HTLV-I immortalized human T-lymphocyte cell line by immunoaffinity chromatography. The tax protein, purified to apparent homogeneity binds to double-stranded DNA irrespective of its origin from either a nuclear or cytoplasmic fraction of the HTLV-I immortalized cell-line - both of which harbor similar quantities of tax protein. The tax protein binds less to single-stranded DNA and not to single-stranded RNA in vitro. It also binds to DNA-cellulose and heparin-Sepharose. Nuclease treatment of isolated nuclei does not release the tax protein under conditions which release known DNA-binding proteins, such as the myb protein. Transactivation by the tax protein presumably involves host-cell factors, since it does not recognize specific DNA sequences.
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PMID:Isolation and characterization of the tax protein of HTLV-I. 278 66

Room temperature fluorescence and low-temperature phosphorescence studies of the association of p10, a basic low molecular weight single-stranded DNA binding protein isolated from murine leukemia viruses, point to the involvement of its single tryptophan residue in a close-range interaction with single-stranded polynucleotides. Optically detected triplet-state magnetic resonance (ODMR) techniques applied to the complex of p10 protein with the heavy atom derivatized polynucleotide poly(5-HgU) demonstrate the occurrence of stacking interactions of Trp35 with nucleic acid bases, thus agreeing with earlier reports that this residue is involved in the binding process [Karpel, R. L., Henderson, L. E., & Oroszlan, S. (1987) J. Biol. Chem. 262, 4961-4967].
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PMID:p10, a low molecular weight single-stranded nucleic acid binding protein of murine leukemia retroviruses, shows stacking interactions of its single tryptophan residue with nucleotide bases. 283 85

There is accumulating evidence for interaction of Epstein-Barr virus (EBV) and human immunodeficiency virus (HIV): EBV and HIV may coinfect B-lymphocytes; the prevalence of active EBV is increased in active homosexuals; and EBV-related B-cell lymphomas occur frequently in AIDS patients. We have shown that cord-blood B-lymphocytes may become infected by HIV once preinfected and transformed by EBV. The present paper, in addition, summarizes mechanisms of transactivation of an HIV LTR construct by an EBV gene product. Also, preliminary data are presented on the activation of an EBV promoter by the human T-cell leukemia virus (HTLV-1).
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PMID:Epstein-Barr virus and interactions with human retroviruses. 284 14

Bovine leukemia virus is the etiological agent of a chronic lymphatic leukemia/lymphoma in cows, sheep, and goats. Infection without neoplastic transformation also was obtained in pigs, rhesus monkeys, chimpanzees, and rabbits, and was observed in capybaras and water buffaloes. Structurally and functionally, BLV is a relative of the human T lymphotropic viruses (HTLV-I and HTLV-II). HTLV-I induces in humans a T cell leukemia, and its type II counterpart has been found in dermatopathic lymphadenopathy, hairy T cell leukemia and prolymphocytic leukemia cases. At variance with HTLV-I, BLV has not been associated with neurological diseases of the degenerative type. BLV, HTLV-I, and HTLV-II show clearcut sequence homologies. The pathology of the BLV-induced disease, most notably, the absence of chronic viremia, a long latency period, and a lack of preferred proviral integration sites in tumors, is similar to that of adult T cell leukemia/lymphoma induced by HTLV-I. The most striking feature of the three naturally transmitted leukemia viruses is the X region located between the env gene and the LTR sequence. The X region contains several overlapping long open reading frames. One of them designated XBL-I encodes a trans-activator function capable of increasing the level of gene expression directed by BLV-LTR and most probably involved in "genetic instability" of BLV-infected cells of the B cell lineage. The genetic instability puts the cell into a context of fragility and ready to move along a number of stages towards full malignancy. Little is known about these events and their causes; we have presented some theoretical possibilities. BLV infection has a worldwide distribution. In temperate climates the virus spreads mostly via iatrogenic transfer of infected lymphocytes. In warm climates and in areas heavily populated by hematophageous insects, there are indications of insect-born propagation of the virus.
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PMID:Bovine leukemia: facts and hypotheses derived from the study of an infectious cancer. 284 1

Human T-cell Leukemia Virus (HTLV-I) gene expression is regulated by both constitutive and inducible enhancer elements. The viral components required for inducible enhancer function include the cis-acting 21 bp motifs present three times within the U3 region of the LTR and the trans-acting 40 kD tax protein encoded by the 3' end of the viral genome. A gel electrophoresis protein-DNA binding assay was used to identify the interaction of nuclear factors with the 21 bp element. Specific protein-DNA interactions were observed in all cell lines examined. No differences were observed in the binding patterns obtained from extracts prepared from those cell lines that did or did not express the tax protein. Dimethyl sulfate (DMS) interference analysis indicates that a nuclear factor contacts the guanine residues in the sequence GGCGTTGAGG. Oligonucleotide directed mutagenesis of the putative protein-DNA contact points markedly reduces the transactivation response. These results support an indirect mechanism for transactivation whereby regulation of HTLV-I gene expression is controlled by the interaction of the cis-acting 21 bp motif with a nuclear factor activated by tax.
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PMID:A nuclear factor is required for transactivation of HTLV-I gene expression. 284 41

We have developed a method for use in investigating factors controlling the binding and cross-linking by bivalent haptens of immunoglobulin E (IgE) bound to receptors on rat basophilic leukemia (RBL) cells. This method employs monoclonal anti-2,4-dinitrophenyl (DNP) IgE that is labeled with fluorescein-5-isothiocyanate (FITC), and it measures FITC quenching that accompanies DNP occupation of the antibody combining sites in a titration experiment. The validity of this approach is demonstrated using the monovalent hapten DNP-L-lysine. The affinity constant for this ligand obtained by the FITC quenching method is compared with those obtained with previously established methods: equilibrium dialysis and quenching of endogenous tryptophan for IgE in solution and [3H]-DNP-L-lysine binding to IgE on cells. The FITC quenching method has been used to carry out a detailed study of the binding of monovalent DNP-aminocapryol-L-tyrosine (DCT) and bivalent (DCT)2-cystine to FITC-IgE and its Fab fragments in solution. Intrinsic (K) and cross-linking (Kx) affinity constants are obtained by analyzing the binding curves in terms of simple equilibrium equations. With these DCT haptens the ability of this method to assess hapten binding and cross-linking of IgE bound to receptors on RBL cells is shown.
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PMID:Cross-linking of IgE-receptor complexes at the cell surface: a fluorescence method for studying the binding of monovalent and bivalent haptens to IgE. 294 10

Early-passaged rat chondroblasts (RX cells) and embryonal fibroblasts (RE cells) are hardly transformed by transfection of activated human H-ras (EJras) or by Abelson murine leukemia virus v-abl oncogene. However, these cells were transformed by v-abl or EJras gene when dexamethasone (DX) was added in the culture medium as well as when co-transfected with retrovirus LTR-linked mouse c-myc gene. RX cell lines carrying v-abl (RXabl), RE cell lines carrying v-abl (REabl) and RX cell lines carrying EJras (RXEJ) were established from transformed colonies in the DX-added soft agar. In the absence and in the presence of DX, RXabl cells showed mortal and immortalized, REabl cells showed mortal and transformed, and RXEJ cells showed immortalized and transformed phenotypes, respectively. Especially, immortalization and transformation of REabl1 and REabl3 lines were switched on and off by addition and depletion of DX. v-abl or EJras mRNA levels in tested REabl, RXabl and RXEJ lines cultured without DX was not decreased compared to those cultured with the hormone. The above suggests that, like myc gene, glucocorticoid collaborates with v-abl or activated ras oncogene to transform unestablished rat cells and that the transformation phenotypes were determined not only by the introduced oncogene but by the cellular condition including their tissue origin. Transformation of senescent REabl cells in the absence of DX was tested by transfecting different oncogenes. Among nuclear oncogenes tested, only adenovirus 12 E1A gene could induce transformation of G0-arrested REabl cells in a cooperative fashion with the integrated v-abl gene.
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PMID:Conditional immortalization and/or transformation of rat cells carrying v-abl or EJras oncogene in the presence or absence of glucocorticoid hormone. 297 44


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