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)

Two types of recombinant vaccinia viruses (VVs) expressing the env gene of the human T-cell leukemia virus type I (HTLV-I) were reported previously. One recombinant VV, WR-proenv1, synthesized the authentic env protein. In the other recombinant VV, WR-env17, the env gene was inserted within the signal sequence of the VV hemagglutinin (HA) gene, so that the reading frame for the env gene was in phase with that for the HA gene. Comparative studies were performed on the mode of expression and processing of the env proteins in relation to their immunogenicity. In WR-env17-infected cells, translation was initiated exclusively from the initiation methionine of the HA to produce nascently the chimeric env protein, including the altered HA signal peptide. Both this altered HA signal peptide and the internalized env signal peptide functioned as insertion signals for the endoplasmic reticulum. Although about half of the nascent chimeric protein was cleaved at the carboxyl terminus of the internalized env signal peptide to produce the authentic env protein, the other half was cleaved at the carboxyl terminus of the altered HA signal peptide alone to synthesize the chimeric protein. These events led to a less efficient transport of the env protein produced by WR-env17 from the rough endoplasmic reticulum to the Golgi apparatus than that of the authentic env protein synthesized by WR-proenv1. The efficiency of the processing and transport of the env protein affected the immunogenicity of these two recombinant VVs.
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PMID:Intracellular processing and immunogenicity of the envelope proteins of human T-cell leukemia virus type I that are expressed from recombinant vaccinia viruses. 218 58

ts1 is a neurovirulent spontaneous temperature-sensitive mutant of Moloney murine leukemia virus TB which causes hindlimb paralysis in mice. Previously, it had been shown that the temperature-sensitive defect resided in the env gene. At the restrictive temperature, the envelope precursor polyprotein, gPr80env, is inefficiently processed intracellularly into two cleavage products, gp70 and Prp15E. This inefficient processing of gPr80env is correlated with neurovirulence. In this study, it was shown that a single amino acid substitution, Val-25----Ile in gPr80env, is responsible for the temperature sensitivity, inefficient processing of gPr80env at the restrictive temperature, and neurovirulence of ts1. At the restrictive temperature, a steady-state level of nonprocessed, endoglycosidase H-sensitive gPr80env remained in the endoplasmic reticulum of cells infected by ts1, but no endoglycosidase H-resistant gPr80env and only trace amounts of gp70 were detected in the infected cells. Since the host cell-encoded processing protease resides in the cis cisternae of the Golgi apparatus, inefficient processing of gPr80env at the restrictive temperature is most likely due to inefficient transport of gPr80env from the endoplasmic reticulum to the cis cisternae of the Golgi apparatus rather than due to misfolded gPr80env being a poor substrate for the processing protease at the restrictive temperature.
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PMID:A Val-25-to-Ile substitution in the envelope precursor polyprotein, gPr80env, is responsible for the temperature sensitivity, inefficient processing of gPr80env, and neurovirulence of ts1, a mutant of Moloney murine leukemia virus TB. 229 75

We report here the establishment of a new cell line, Karpas 620 (K620), from the peripheral blood of an elderly woman with an IgG-kappa plasma cell leukaemia (PCL). The line has the same hypotetraploid karyotype as the fresh cells from the patient. The cultured cells have the ultrastructural appearance of plasma cells with abundant rough endoplasmic reticulum (RER) and secrete kappa light chain. They are positive for surface antigens HLA DR, and WR17 (CD 37) and negative for CD1, CD3, CD4 and CD8. Using high resolution (HR) cytogenetic analysis it has been possible to identify all the marker chromosomes including several rearrangements commonly seen in malignancies of B cell lineage. These are a 14q+ marker with a typical 'Burkitt' morphology der(14)(pter----q32.3::8q24.1----qter) but with no reciprocal 8q-, and three translocations involving chromosome 11 at q13 with partners other than chromosome 14, namely 1q32.1, 8q24.22 and 13q14.3. An earlier report of molecular studies on the DNA of K620 has shown a rearrangement near the region on 11q13 designated BCL-1 (Rabbitts et al. 1988). This is the first report of a rearrangement in the region of 11q13 in a cell line originating from a case of plasma cell leukaemia.
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PMID:A new human plasma cell line, Karpas 620, with translocations involving chromosomes 1, 11 and 14. 231 Jun 98

Activity of a chymotrypsin-type serine protease was found in a subline of rat basophilic leukemia (RBL-2H3) cells. The protease was immunologically cross-reactive with anti-atypical mast cell protease immunoglobulin (Ig) G, and its activity was inhibited in a dose-dependent manner by the antibody. The apparent m.w. of the protease that reacted with the antibody was 25,000, which was identical with that of atypical mast cell protease in rat mucosal mast cells. These results show that the chymotrypsin type serine protease in RBL-2H3 cells is immunologically identical with atypical mast cell protease, which was first purified from rat small intestine. Immunohistochemical studies showed that the protease was located not only in intracytoplasmic granules but also in organelles synthesizing protein, such as cisternae of the rough endoplasmic reticulum, perinuclear spaces, and the Golgi apparatus. However, no immunoreactivity was demonstrated in rat basophils. The activity of the protease increased in the exponential phase of growth of RBL-2H3 cells in which some activity was also detected in the medium, and it decreased in the late stationary phase.
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PMID:A chymotrypsin-type serine protease in rat basophilic leukemia cells: evidence for its immunologic identity with atypical mast cell protease. 241 25

By electron microscopy and immunocytochemistry we have examined the retroviruses endogenous to AtT20 D16V cells, a cloned line of murine pituitary tumour cells. In addition to the C-type retrovirus particles related to Rauscher murine leukemia virus (MuLV) previously reported to bud from these cells we observed cytoplasmic A-type particles and intracisternal A-type particles (IAP). In the cytoplasm the A-type particles occur in large clusters often associated with sheets of material with a fine structure resembling the shells of the particles. At the plasma membrane individual A-type particles bud to give rise to extracellular virions. The IAP are restricted to the rough endoplasmic reticulum (RER) into which they bud: they are not transported out of the RER to the Golgi apparatus and beyond. We describe a new monoclonal antibody (designated 83E7) which is specific for an epitope of the major core protein (MTVp27) of mouse mammary tumour virus (MMTV). Using immunogold labelling procedures we have specifically labelled both the A-type particles and the associated sheets of material with this antibody. We conclude that the A-type particles and the virions they give rise to are MMTV. The sheets of material must also at least in part be made up of the major core protein of MMTV or its precursor polypeptide. AtT20 cells, therefore, contain endogenous MuLV and MMTV as well as IAP.
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PMID:AtT20 pituitary tumour cells contain mouse mammary tumour virus and intracisternal A-type particles in addition to murine leukemia virus. 241 43

A patient with chronic B-cell leukemia in whom the malignant lymphocytes showed intracellular inclusions of immunoglobulin (Ig) G kappa molecules is described. Electron microscopy revealed filamentous material in the nuclear envelopes and in the cisternae of the rough endoplasmic reticulum. These in vivo surface Ig-negative, nonexcreting cells could be stimulated in vitro to excrete immunoglobulin-free light chain molecules into the supernatant, which were not found in the cytoplasm after stimulation.
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PMID:Intracellular immunoglobulin G 'pseudocrystals' in a patient with chronic B-cell leukemia. 242 26

A new megakaryoblastic cell line (CMK), which also exhibits erythroid and myeloid markers, was established from a Down's syndrome patient suffering from acute megakaryoblastic leukaemia. The CMK cells were found to be positive in reactions with anti-platelet antibodies (anti-glycoproteins IIb/IIIa and Ib, and Plt-1). Platelet peroxidase (PPO) reactivity was found to be associated with the nuclear envelope and the endoplasmic reticulum but not with the Golgi apparatus. Some cells possessed cytoplasmic granules with the characteristics of alpha-granules and demarcation membranes. Karyotyping revealed near-tetraploidy (modal chromosome number of 95; ranging 87-98) and a translocation der(17)t(11;17), also found in the original leukaemic cells, confirming that the cells were derived from the patient's malignant blasts. The CMK cells were also found to be positive in reaction with anti-glycophorin A antibody, as well as with anti-myeloid antibodies (MY4, MY7 and MY9). Treatment of CMK cells with phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) greatly enhanced the reactivity with anti-platelet antibodies, increased the number of cells in which cytoplasm was dissociated into numerous segments and suppressed the reactivity with anti-glycophorin A. The proliferation of CMK cells was stimulated by interleukin-3 (IL-3) and granulocyte-macrophage colony stimulation factor (GM-CSF). This cell line should be a useful tool for analysing the basis of the afferent association between megakaryoblastic leukaemia and Down's syndrome, as well as for further study of megakaryocytic differentiation.
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PMID:Establishment of a human leukaemic cell line (CMK) with megakaryocytic characteristics from a Down's syndrome patient with acute megakaryoblastic leukaemia. 252 57

In order to study the relationship between assembly, surface expression, and signal transduction of the alpha/beta T-cell antigen receptor-CD3 complex (TCR.CD3), a series of T-cell mutants with a partial block in assembly of the complex was generated. By chemical mutagenesis, we produced somatic cell variants of the human T-leukemia cell line, HPB-ALL, which expressed low amounts of TCR.CD3 complexes on their surface. RNA and protein analyses demonstrated that most variants synthesized normal amounts of the individual members of the complex, i.e. TCR-alpha, TCR-beta, CD3-gamma, -delta, -epsilon, and -zeta. In these variants, less than 10% of the TCR.CD3 complexes inside the cell contained the CD3-zeta 2 homodimer due to an intrinsic deficiency in the formation of the TCR-alpha/beta heterodimer. The low level of assembly of CD3-zeta 2 into the TCR.CD3 complex and an additional decrease in the rate of export of the TCR.CD3 complex from the endoplasmic reticulum explained the low level of expression of alpha/beta receptors on the surface of these mutants. Only cells with the complete set of subunits of the TCR.CD3 complex on their surface were capable of transducing CD3-mediated signals. The results presented in this paper indicate that TCR-alpha/beta heterodimer formation is an obligatory requirement for assemblage of CD3-zeta 2 into a functionally competent TCR.CD3 complex.
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PMID:T-cell antigen receptor (TCR)-alpha/beta heterodimer formation is a prerequisite for association of CD3-zeta 2 into functionally competent TCR.CD3 complexes. 253 Nov 45

Cytoplasts (plasma membrane sacs containing cytoplasm, endoplasmic reticulum, and few organelles) were prepared from rat basophilic leukemia cells by treatment with cytochalasin B and centrifugation at 33 degrees C through stepwise gradients of Ficoll. To compare the relative ability of cytoplasts and cells to generate second-messengers (inositol phosphates, Ca2+) in response to stimulation of the high affinity receptor for IgE, we normalized our results per recovered receptor by using the tightly bound IgE as a marker. This marker correlated well with other estimates of plasma membrane recovery. Furthermore, data normalized on this basis correlated well with data expressed as percentage of phosphoinositides hydrolyzed. The purest fraction of cytoplasts (containing about 6% of the receptors) was satisfactorily devoid of organelles and, at early times, generated about 50% as much inositol phosphates per receptor as did the intact, untreated cells. This response of the cytoplasts, like that of the cells, was totally dependent upon aggregation of the receptors. The response by the cytoplasts (in the 5-min time frame which we examined), unlike that of the cells, was not enhanced by the presence of extracellular Ca2+. Furthermore, unlike the cells, the cytoplasts failed to raise their intracellular free Ca2+ levels after addition of polyvalent Ag. This result suggests that aggregation of the receptors may be insufficient, by itself, to open the normal Ca2+ channels.
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PMID:IgE receptor-mediated hydrolysis of phosphoinositides by cytoplasts from rat basophilic leukemia cells. 254 11

An analysis of the human leukemia cell line, K-562, infected with Semliki Forest virus, has been made with transmission electron microscopy. In contrast to the usual surface budding of the enveloped virus on the plasma membrane of vertebrate cells leading to cytolysis within 20 h, K-562 cells do not show surface budding, and the cells remain intact for periods of several months. Several unusual features of the infection include: 1) the rough endoplasmic reticulum arranges early into continuous perinuclear chains; 2) during the time of virus replication and release, the nucleocapsids aggregate on the cytoplasmic side of internal vesicles in the region of the cell where the Golgi complex is normally located; and 3) during this same time period, the vesicles are seen to contain enveloped virions and rod-like formations, a result suggesting that budding has occurred into these vesicles. Viruses are presumably released from the cell as these vesicles fuse with the plasma membrane. By 12 days post-infection and thereafter, the intact cells show electron-dense aggregates of chromatin, large vacuoles and lipid inclusions throughout the cytoplasm, and only a few virion-containing vesicles.
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PMID:Involvement of cytoplasmic membranes in the non-lytic infection of K-562 cells by Semliki Forest virus. 254 48


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