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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

DNA replication blockage in various differentiated cells was investigated on the model of heterokaryons. Two distinct types of DNA synthesis regulation in heterokaryons "differentiated cell + proliferating cell" were revealed: I. Neutrophils and nucleated erythrocytes efficiently prevented the entry of non-malignant proliferating cells nuclei into the S-period but usually failed to substantially inhibit the replication in malignant cells nuclei. Both "mortal" and immortalized proliferating cells activated the DNA synthesis in neutrophil and chicken erythrocyte nuclei. II. Macrophages did not influence the DNA synthesis in the nuclei of non-malignant cells in heterokaryons but drastically inhibited that in the nuclei of malignant cells. Only immortalized cells reactivated DNA synthesis in the nuclei of macrophages. These data show that the mechanisms maintaining differentiated cells in non-proliferating state are not uniform. Nucleated erythrocytes were shown to suppress the duplication of centrioles in partner cells. The possibility of the blockage of DNA replication upon the fusion of two proliferating cells (fibroblast + leukemia cell) was demonstrated for the first time in the present work. The influence of various oncogenes upon the regulation of DNA synthesis in heterokaryons was investigated in detail. New modifications of the methods of cell fusion, enucleation and heterokaryon identification were proposed.
Mol Biol (Mosk)
PMID:[Positive and negative regulation of replication in hybrid cells]. 172 75

In Moloney murine leukemia virus, the encapsidation Psi element was shown to be necessary and sufficient to promote packaging of viral RNA, and to be required for dimerization. The conformation of the Psi domain (nucleotides 215 to 565) was investigated in solution by chemical probing. The four bases were monitored at one of their Watson-Crick positions with dimethylsulfate at cytosine N3 and adenosine N1, and with a carbodiimide derivative at guanosine N1 and uridine N3. Position N7 of adenine residues was probed with diethylpyrocarbonate. The analyses were conducted on in vitro transcribed fragments corresponding either to the isolated Psi domain or to the 5'-terminal 725 nucleotides. The RNA fragments were analyzed in their monomeric and dimeric forms. A secondary structure model was derived from probing data, computer prediction and sequence analysis of related murine retroviruses. One major result is that Psi forms an independent and highly structured domain. Dimerization induces an extensive reduction of reactivity in region 278 to 309 that can be interpreted as the result of intermolecular interactions and/or intramolecular conformational rearrangements. A second region (around position 215) was shown to display discrete reactivity changes upon dimerization. These two regions represent likely elements of dimerization. More unexpectedly, reactivity changes (essentially enhancement of reactivity) were also detected in another part of Psi (around position 480) not believed to contain elements of dimerization. These reactivity changes could be interpreted as dimerization-induced allosteric transitions.
J Mol Biol 1992 Jan 05
PMID:Effect of dimerization on the conformation of the encapsidation Psi domain of Moloney murine leukemia virus RNA. 173 Oct 69

Lymphotoxin (LT; also known as tumor necrosis factor-beta) is a pleiotropic cytokine whose expression is tightly regulated in most cells and is repressed prior to activation signals. In some early B cells and Abelson murine leukemia virus-transformed pre-B-cell lines, LT mRNA is constitutively expressed. To examine the molecular regulation of the LT gene in a constitutively expressing cell line, we studied the Abelson murine leukemia virus-transformed lines PD and PD31. As demonstrated by primer extension analysis, constitutively expressed pre-B-cell-derived and inducibly expressed T-cell-derived LT mRNA were initiated at the same cap sites and predominant cap site utilization was conserved. Furthermore, we delineated an upstream activating sequence that was an important functional component of lymphotoxin transcriptional activation in PD and PD31 cells. The upstream activating sequence was localized to an essentially homopolymeric A + T-rich region (LT-612/-580), which was bound specifically by recombinant human high-mobility group I protein (HMG-I) and a PD/PD31 nuclear extract HMG-I (HMG-I-like) protein. The nuclear extract-derived HMG-I-like protein was recognized by anti-HMG-I antibody and bound to LT DNA to effect an electrophoretic mobility shift identical to that of bound recombinant human HMG-I. These findings implicate HMG-I in the regulation of constitutive lymphotoxin gene expression in PD and PD31 cells. HMG-I and HMG-I-like proteins could facilitate the formation of active initiation complexes by altering chromatin structure and/or by creating recognition sites for other activator DNA-binding proteins, some of which may be unique to or uniquely modified in these constitutive LT mRNA producers.
Mol Cell Biol 1992 Feb
PMID:A poly(dA-dT) upstream activating sequence binds high-mobility group I protein and contributes to lymphotoxin (tumor necrosis factor-beta) gene regulation. 173 52

The role of restricted cellular accumulation of cis-diamminedichloroplatinum(II) (cis-DDP) and altered repair of DNA-Pt-protein cross-links in the mechanism of L1210 murine leukemia cell resistance was examined. An immunochemical method was used to analyze the formation and removal of DNA-Pt-protein complexes in L1210 cells sensitive and resistant to cis-DDP. The accumulation of Pt into the cells and the binding of Pt to the DNA was measured by atomic absorption spectroscopy. The results demonstrated that both decreased accumulation of the drug and the rate of DNA-Pt protein cross-link removal may be important factors in L1210 cell resistance to cis-DDP.
Mol Biol Rep 1991 May
PMID:DNA-protein cross-linking in L1210 cells sensitive and resistant to cis-diamminedichloroplatinum (II). 174 77

Normal feline bone marrow-derived macrophages released maximum concentrations of interleukin-6, tumor necrosis factor, and interleukin-1 when stimulated with ImuVert (Cell Technology Inc, Boulder, CO, USA) at dosages of 1.0 microgram/ml, 5.0 micrograms/ml, and 10.0 micrograms/ml, respectively. When ImuVert was administered to healthy adult cats, significant elevations in rectal temperature and neutrophil counts were observed 10 and 24 hours after each treatment. Weekly treatment with ImuVert failed to prevent or reverse viremia in cats when initiated prior to or 6 weeks after inoculation with feline leukemia virus.
Mol Biother 1991 Dec
PMID:Evaluation of a biologic response modifier derived from Serratia marcescens: effects on feline macrophages and usefulness for the prevention and treatment of viremia in feline leukemia virus-infected cats. 176 75

The constitutive expression of 25-hydroxyvitamin D3-24-hydroxylase (25-(OH)D3-24-hydroxylase) activity has been studied in an adherent variant (Ad-HL60) of the human promyelomonocytic leukaemia cell line HL60. The Ad-HL60 cells have a more differentiated phenotype than the non-adherent cells from which they were derived, and synthesized 1.88 +/- 0.07 (+/- S.E.M.) pmol 24,25-(OH)2D3/h per 10(6) cells following culture in RPMI-1640 medium containing less than 0.02 nM 1 alpha,25-(OH)2D3. They also synthesized 1.66 +/- 0.05 pmol 24,25-(OH)2D3/h per 10(6) cells following culture in 1 alpha,25(OH)2D3-free medium supplemented with 1 g bovine serum albumin/l instead of 10% serum. In contrast, non-adherent HL60 cells required exposure to 10-100 nM 1 alpha,25-(OH)2D3 to induce equivalent 24,25-(OH)2D3 synthesis. The 25-(OH)D3-24-hydroxylase expressed by Ad-HL60 cells had an apparent Michaelis constant of 1 microM and maximal rate of 20 pmol/h per 10(6) cells with substrate concentrations from 0.012 to 1.2 microM/incubation (5-500 ng/ml). Furthermore, 24,25-(OH)2D3 synthesis was inhibited in a dose-dependent manner by ketoconazole (0.01-10 microM), suggesting that the enzyme is cytochrome P-450 dependent. Ad-HL60 cells expressed approximately 3500 specific receptors for 1 alpha,25-(OH)2D3/cell with a dissociation constant of 40 pM. Following exposure to 0.1-100 nM 1 alpha,25-(OH)2D3, Ad-HL60 cell proliferation was significantly inhibited compared with controls grown in medium containing less than 0.02 nM 1 alpha,25-(OH)2D3 for 96 h. Expression of 25-(OH)D3-24-hydroxylase was also inhibited in a dose- and time-dependent manner; however, expression of nonspecific esterase was not induced. Both of these findings are contrary to those previously demonstrated for non-adherent HL60 cells, whereas the dose-dependent inhibition of cell proliferation by 1 alpha,25-(OH)2D3 occurs in both adherent and non-adherent phenotypes. These observations on Ad-HL60 cells represent the first description of a cell type in which 1 alpha,25-(OH)2D3 appears to inhibit 25-(OH)D3-24-hydroxylase activity. The Ad-HL60 cells also constitutively metabolized 1 alpha,25-(OH)2D3 in a manner consistent with formation of 1 alpha,25-(OH)2D3 without previous exposure to 1 alpha,25-(OH)2D3. In contrast, many other cell types, including non-adherent HL60 cells, require exposure to 1 alpha,25-(OH)2D3 to induce metabolism of 1 alpha,25-(OH)2D3 to 1 alpha,24,25-(OH)3D3, a reaction that represents the initial step for catabolism of 1 alpha,25-(OH)2D3 to calcitroic acid.
J Mol Endocrinol 1991 Dec
PMID:Studies on an adherent variant of the human promyelomonocytic HL60 leukaemia cell line that constitutively expresses 25-hydroxyvitamin D3-24-hydroxylase activity which is inhibited by 1 alpha,25-dihydroxyvitamin D3. 177 40

We studied the seroconversion to human T-cell leukemia virus type-1 (HTLV-I) in two immunocompromised patients after transfusions of cellular blood components. One patient produced IgM antibodies against the viral p19 protein 149 days post-transfusion (a serum on day 43 was negative). Both patients showed indeterminate Western-blots (IgG anti-p19 and anti-gp46 but no anti-p24). Using the polymerase chain reaction (PCR) with two primer pairs (SK43/44 and SK54/56), we demonstrated HTLV-I infection prior to seroconversion. This infection was confirmed by Southern blot.
Mol Cell Probes 1991 Oct
PMID:Use of PCR amplification for diagnosis of HTLV-I infection after blood transfusion. 179 55

In the maximum likelihood (ML) method for estimating a molecular phylogenetic tree, the pattern of nucleotide substitutions for computing likelihood values is assumed to be simpler than that of the actual evolutionary process, simply because the process, considered to be quite devious, is unknown. The problem, however, is that there has been no guarantee to endorse the simplification. To study this problem, we first evaluated the robustness of the ML method in the estimation of molecular trees against different nucleotide substitution patterns, including Jukes and Cantor's, the simplest ever proposed. Namely, we conducted computer simulations in which we could set up various evolutionary models of a hypothetical gene, and define a true tree to which an estimated tree by the ML method was to be compared. The results show that topology estimation by the ML method is considerably robust against different ratios of transitions to transversions and different GC contents, but branch length estimation is not so. The ML tree estimation based on Jukes and Cantor's model is also revealed to be resistant to GC content, but rather sensitive to the ratio of transitions to transversions. We then applied the ML method with different substitution patterns to nucleotide sequence data on tax gene from T-cell leukemia viruses whose evolutionary process must have been more complicated than that of the hypothetical gene. The results are in accordance with those from the simulation study, showing that Jukes and Cantor's model is as useful as a more complicated one for making inferences about molecular phylogeny of the viruses.
J Mol Evol 1991 Jan
PMID:Robustness of maximum likelihood tree estimation against different patterns of base substitutions. 184 80

The administration of the DNA topoisomerase II inhibitors 4'-(9-acridinylamino)methanesulfon-m-anisidide (m-AMSA) (10(-7) M), VP-16 (2 x 10(-7) M), or novobiocin (1.5 x 10(-4) M) reduces the growth activity of human promonocytic leukemia U-937 cells, by arresting them preferentially at the G2 (m-AMSA and VP-16) or at the G1 and G2 (novobiocin) phases of the cell cycle. Under these conditions, m-AMSA and VP-16 induce the differentiation of the cells efficiently, as proved both by an increase in the production of reactive oxygen species and by the activation of the surface expression of CD11b and CD11c, two differentiation-specific antigens. Novobiocin also induces the expression of those differentiation markers, but to a lesser extent. Analyses by Northern blot indicate that the topoisomerase II inhibitors reduce the levels of c-myc and beta-actin mRNA and increase the levels of vimentin mRNA. The expression of vimentin is also stimulated at the protein level, as indicated by immunofluorescence assays. This represents one of the few known instances in which topoisomerase inhibitors stimulate gene expression in eukaryotic cells.
Mol Pharmacol 1991 Apr
PMID:Differentiation of human promonocytic leukemia U-937 cells with DNA topoisomerase II inhibitors: induction of vimentin gene expression. 185 89

Serotonin release from rat basophilic leukemia (RBL) cells, sensitized with a DNP-binding monoclonal IgE, was stimulated with solid surface (polystyrene)-bound DNP-amino acids. The stimulatory potency of DNP-amino acids was dependent on the structure of amino acid attached to DNP. Generally, DNP-amino acids with high affinities to the sensitizing IgE (I(50) less than 10 microM) were stimulatory in polystyrene-bound form; DNP-amino acids with lower affinities (Pro, Cys, Trp), and aliphatic aromatic DNP-amino acid derivatives were inactive. In addition to structural analogues of DNP, lymecycline, that is chemically unrelated to DNP but was found to have high affinity to IgE(aDNP), was also stimulatory in this system. This drug, and various quinones (e.g. acenaphthene-quinone) in BSA-conjugated forms also stimulated serotonin release from RBL cells sensitized with IgE(aDNP). These studies suggest that (1) There is a threshold of intrinsic ligand binding affinities at approximately I(50) = 10-100 microM; ligands with lower affinities do not stimulate mediator release even if they are presented in multivalent forms; (2) The above affinity threshold for mediator cell stimulation is valid for various ligands, irrespective of their chemical similarity to the immunogen; (3) Multispecific stimulation of mediator release may contribute to the frequently observed allergic cross-reactions, false positive tests for allergies, and anaphylactic reactions to drugs upon first exposure.
Mol Immunol 1991 Jun
PMID:Mechanism of allergic cross-reactions--II. Cross-stimulation, by chemically unrelated ligands, of rat basophilic leukemia cells sensitized with an anti-DNP IgE antibody. 186 80


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