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)

The present study investigates the fate of the cell-bound IgE by using a well-characterized rat basophilic leukemia cell line and a purifed IgE myeloma protein. Both histamine-releasing and nonreleasing cell lines were examined. In both cases, no evidence for cell-mediated IgE catabolism could be elicited. Both the dissociated IgE and the receptors remained intact for prolonged periods of time, as demonstrated by binding assays. Internalization and/or recycling of membrane-bound IgE could not be demonstrated by E. M. autoradiography. We found only limited time-dependent changes in accessibility to anti-IgE antibody, trypsin, or elution at low pH (2.9 to 3.1). A biphasic dissociation of cell-bound 125I-IgE during incubation in the presence of excess unlabeled IgE was reproducibly observed; the more slowly dissociated IgE was also less readily dissociated at pH 3.4. These studies lead us to conclude that, in vitro, IgE resides in a functional orientation on the surface of RBL-1 cells, for prolonged periods of time.
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PMID:The fate of IgE bound to rat basophilic leukemia cells. 3 32

The availability of a patient with basophilic leukemia manifesting 75 to 90% mature basophils permitted the use of a cell concentration sufficient to generate and release mediators upon interaction with a calcium ionophore in quantities adequate for their physiocochemical characterization. The mediators were defined in terms of their physicochemical characteristics: slow reacting substance of anaphylaxis (SRS-A) by purification through silicic acid chromatography and inactivation by arylsulfatase; eosinophil chemotactic factor of anaphylaxis (ECF-A) by its gel filtration through Sephadex G-25 and inactivation by subtilisin and not trypsin; and platelet-activating factor (PAF) by its inherent binding to albumin. Both ECF-A and histamine were present in their preformed state, and for histamine it was possible to establish that the concentration per cell was comparable to that of normal human basophils. Dibutyryl cyclic AMP suppressed release of histamine and SRS-A, indicating that their availability was under a control similar to that observed with normal cells subjected to immunologic activation. The demonstration that a suspension of leukemic human basophils contained the preformed mediators, histamine and ECF-A, and generated SRS-A and PAF for release along with histamine and ECF-A, after activation with a calcium ionophore, establishes that a single cell type can serve as a source of the four recognized mediators of immediate-type hypersensitivity.
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PMID:The release of four mediators of immediate hypersensitivity from human leukemic basophils. 4 47

A 60,000-dalton polypeptide (p60) has been identified in the feline leukemia virus (FeLV) pseudotype of Moloney sarcoma virus [MSV(FeLV)]. This polypeptide is present in the purified virus complex in concentrations greater than either the murine p30 or the feline p27. Purified p60 crossreacts immunologically with murine p30 group antiserum and contains several interspecies determinants, whereas the group specific determinant of FeLV p27 is not detected. Comparison of peptide fingerprints of p60 and murine p30 show many peptides in common. Limited digestion of p60 with either trypsin or chymotrypsin produced p30-35 and p20 peptides which retain the MuLV p30 group and interspecies antigenic activities. The p30 produced by both enzymes comigrates in polyacrylamide gels with the murine p30 of MSV(FeLV), thus suggesting that p60 may be an uncleaved precursor to p30.
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PMID:A p60 polypeptide in the feline leukemia virus pseudotype of Moloney sarcoma virus with murine leukemia virus p30 antigenic determinants. 4 60

Cells from several mouse lymphomas formed rosettes with nonsensitized foreign erythrocytes through C-type virus particles clustered on the cell surface in serum-free medium held at 4 degrees C. This type of rosetting was found most typically in a lymphoma induced by Rauscher leukemia virus in tissue culture (RD-12), but it also occurred in 23 of 61 spontaneous thymic lymphomas in AKR mice. Chemically or X-ray-induced leukemias and spontaneous reticulum cell sarcomas did not form rosettes. The nature of the rosette formation may be interpreted as viral hemadsorption, with a possible relationship to hemagglutination by murine leukemia viruses. The receptor on virus particles was trypsin sensitive and showed high affinity to serum inhibitors (RIF). Serum rosette-inhibiting activity was assessed by a quantitative rosette inhibition test; rosette inhibition proved widely distributed among species. Physicochemical properties of serum RIF and their function both in vivo and in vitro were described. Rosette formation with similar temperature requirements, previously reported in a mouse lymphoma carrying membrane-bound heterophile cold hemagglutinin, was readily distinguished from viral hemadsorption by its insensitivity to mouse serum RIF.
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PMID:Temperature-dependent rosette formation by mouse lymphoma cells as a result of viral hemadsorption. 5 22

We have used a quantitative radiolabelled antibody procedure to measure the amount of certain virus structural antigens on the surface of BALB/c RAG cells producing endogenous B-tropic type C virus. RAG cells expressed group specificities of MuLV p30 on their cell surface but did not express gp70 group specificities. However, type specificities of gp70 were expressed on BALB/c cell lines infected with Moloney leukaemia virus. The majority of p30 antigens detected on the RAG cell surface were removed by trypsin and their reappearance was prevented by cycloheximide, even in the presence of 'conditioned medium' containing MuLV. Passive adsorption of exogenous MuLV p30 to the surface of virus negative BALB/c fibroblasts reached a maximum of 20% of the protein detectable on virus producing RAG cells. These data support the hypothesis that much, but not all, of the surface p30 is expressed de novo on the cell membrane and not derived from passive adsorption of p30 released from shed virus or as a by-product of virus infection of a cell.
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PMID:Expression of virus structural proteins on murine cell surfaces in association with the production of murine leukaemia virus. 6 22

Murine leukemia viruses, such as Rauscher leukemia virus (RLV), contain a proteolytic factor which becomes activated after detergent treatment of the virus. This factor specifically cleaves P70, the gag precursor polyprotein which is enriched for in preparations of immature virus core subparticles. The factor has been partially purified on Sephadex G-75 columns. It has a molecular weight of 10,000-12,000 daltons but does not coincide in elution position with the major peaks of the viral polypeptides p10 or p12. Under optimal conditions, that is 2% NP-40 (v/v), 10 mM DTT, (pH 7.2) and incubation for 16 hr at 22 degrees C, cleavage of labeled P70 occurs and increasing amounts of the four gag polypeptides p30, p15, p12 and p10 are obtained. The P70 cleavage activity is blocked by TLCK, TAME, CBZ-lysine and other lysyl-containing protease inhibitors. Further, the CBZ-lysine inhibition is reversible, while an inhibition by phenyl-methylsulfonyl fluoride (PMSF) is irreversible. These inhibition studies suggest that a similarity exists between the P70 proteolytic factor and some serine proteases, such as trypsin. The cleavage pattern of P70-rich immature cores treated with trypsin or chymotrypsin is different from that obtained with the P70 proteolytic factor. Thus murine leukemia virions apparently contain a unique, highly specific protease which is present in small amounts and cleaves P70.
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PMID:Properties of a P70 proteolytic factor of murine leukemia viruses. 7 13

Plasma membranes were isolated from the leukemia cell line ASL1w and extracted with detergent (DOC). DOC solubilized more TL activity than could be detected on isolated membranes. However, extraction of membranes with LDS or EDTA solubilized only 17% and 4%, respectively, of the activity. This indicated that TL was not loosely associated with the membrane but rather was integrated into the lipid bilayer. At low concentrations of DOC (0.05%), TL was found to be largely aggregated and was also prone to autolysis. Neither aggregation nor autolysis was observed at a higher DOC concentration (0.5%). The apparent molecular weight of TL in 0.5% DOC was determined by Sephadex G-200 chromatography to be about 65,000-70,000. Digestion of a 0.5% DOC extract of TL with either papain or trypsin produced a fragment of TL of about 35,000 molecular weight. These fragments were similar in size to a fragment produced by autolysis. These data suggested that a region of the TL molecule was very prone to proteolytic attack. The 35,000 molecular weight proteolytic fragments bound specifically to lentil lectin affinity columns, which indicated that they retained at least part of the carbohydrate present on the native molecule.
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PMID:Some structural properties of thymus leukemia antigen (TL) solubilized with detergent. 9 17

Changes of prekallikrein in the cases with DIC were investigated, i.e., DIC cases including disseminated metastasis of gastric cancer, acute promyelocytic leukemia and endotoxin shock. Therefore, the trigger substances for this paper were the pathologic cells of the leukemia, the cultured well differentiated adenocarcinoma cells and endotoxin. (1) The lysates of the pathologic cells of the leukemia and the cultured cells showed prekallikrein activation. Endotoxin showed prekallikrein activation via factor XII. (2) Serine proteases (factor Xa, thrombin, plasmin and trypsin) activated prekallikrein in the plasma and the purified prekallikrein. (3) Antithrombin III, aprotinin and FOY inhibited prekallikrein activation. Antithrombin III was promoted by heparin in its inhibitory effect.
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PMID:Changes of prekallikrein in the cases with disseminated intravascular coagulation syndrome. 16 Jan 91

Primary cell cultures of mammary tumors from Rill, GR, DD, BALB/cfC3H, and BALB/c mice were prepared by trypsin-EDTA dissociation of tumors. Cultures from these strains contained predominantly cells of epithelial morphology which formed three-dimensional domelike structures. Cultures from Rill, GR, DD, and BALB/cfC3H tumors produced extra-cellular type-B mouse mammary tumor virus(es) (MuMTV), either in the absence of detectable type-C virus or with less than 1% contamination with type-C virus. This was determined by radioimmunoassays for MuMTV and murine leukemia virus (MuLV) antigens. Only BALB/c cultures produced MuMTV with as much as 3% contaminating MuLV. High levels of MuMTV surface antigen were also found in soluble form in culture supernatants. Virus polypeptide analyses by electrophoresis on polyacrylamide gels showed that the Rill BALB/cfC3H, DD, and BALB/c viruses all contained polypeptides characteristic of MuMTV. Primary cultures of mammary tumor cells make available a source of purified MuMTV antigens, structural proteins, and nucleic acids for comparative studies of MuMTV from various mouse strains.
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PMID:Characterization of mouse mammary tumor viruses from primary tumor cell cultures.I. Immunologic and structural studies. 17 73

Concentrated murine leukemia virus (MuLV) or MuLV producing cells induce XC cell fusion within an hour leading to syncytia formation. While MuLV inactivated by UV irradiation, beta-propiolactone or hydroxylamine treatment still caused cell fusion, Bromelin- or trypsin treated MuLV was no longer able to fuse XC cells. Though sonicated MuLV induced no XC cell fusion, it interfered with cell fusion as caused by untreated MuLV. XC cells infected by diluted MuLV of a titer lower than 1 X 10(5) PFU/ml formed no syncytia although they produced MuLV. The cell fusion mechanism is discussed.
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PMID:XC cell fusion by murine leukemia viruses: fusion from without. 18 16


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