Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The heterogeneity of Epstein-Barr virus (EBV) obtained from P3HR-1 cells has permitted derivation of a distinct subclone of P3HR-1 (L. Heston, M. Rabson, N. Brown, and G. Miller, Nature (London) 295:160-163, 1982). We have analyzed the biologic properties and genomic structure of this subclonal virus (clone 13) compared with those of parental P3HR-1 and B95-8 viruses. Synthesis of EBV compared with those of parental P3HR-1 and B95-8 viruses. Synthesis of EBV proteins in Raji cells superinfected with virus derived from P3HR-1, clone 13, and B95-8 was analyzed both by fluorography of radiolabeled proteins and by immunoblotting. Highly concentrated preparations of clone 13 and B95-8 virus induced most of the spectrum of EBV proteins in Raji cells with the exception of the 145,000-, 140,000-, and 110,000-molecular-weight proteins, which were either undetectable or reduced. Moreover, both clone 13 and B95-8 viruses also induced the same patterns of early antigen diffuse components as the parental P3HR-1 virus did. However, only P3HR-1 virus could induce EBV DNA synthesis in superinfected Raji cells, as determined both by buoyant density centrifugation and by in situ cytohybridization with biotinylated recombinant EBV DNA probes. Defective heterogeneous molecules present in P3HR-1 virus have been implicated in early antigen induction after superinfection of Raji cells. Therefore, Southern blots of clone 13, P3HR-1, and B95-8 viruses were hybridized to recombinant EBV fragments representing the sequences contained within the defective molecules in P3HR-1. The parental P3HR-1 contained the previously described defective molecules. No evidence for defective molecules was found in clone 13 or B95-8 viruses. These data indicate that concentrated preparations of both clone 13 and B95-8 viruses can induce abortive infection in Raji cells, but while the defective molecules are not needed for induction of early antigen diffuse components, they may be required for the induction of viral DNA synthesis.
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PMID:Two strains of Epstein-Barr virus (B95-8 and a P3HR-1 subclone) that lack defective genomes induce early antigen and cause abortive infection of Raji cells. 303 25

Brown-Norway rats maintained under conventional housing conditions showed a significant increase in the C1q binding activity of serum and to a lesser extent of the Raji cell assay whereas no change was observed, in BN rats maintained under specific pathogen free (SPF) conditions. Glomerular IgG deposits were encountered among rats with circulating immune complexes (CIC). This suggests that microbiological environment is a major factor in the spontaneous appearance of CIC which could be of pathogenic significance.
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PMID:Spontaneous circulating immune complex like material in Brown-Norway rats. Role of environmental factors. 621 76

Immune complexes (IC) were detected and isolated from the serum of Brown Norway (BN), (Lewis x BN)F1, and Lewis rats bearing a Moloney sarcoma (MST). IC were isolated from the serum of individual rats employing a system of G-200 chromatography and passage through a heavy chain specific anti-rat IgG Immunoadsorbent. IgG and IgM were identified in the isolated IC by polyacrylamide gel electrophoresis (PAGE) and co-precipitation radioimmunoassays. Employing monospecific antibodies, IC consisting of IgG and IgM were bound to Raji cells as assessed by radioimmunoassay and indirect immunofluorescence. Raji binding activity of IC-containing serum was substantially reduced by pretreatment with dithiothreitol or incubation with anti-rat IgM or pooled normal rat IgG: F(ab')2. Sucrose density gradient ultracentrifugation under acid conditions dissociated IC into 7S IgG and 19S IgM components which recombined when co-incubated at pH 7 . 5. Viral antigens (gp70 and p30) were not detected in IC by PAGE and co-precipitation radioimmunoassay. Findings show that sera of rats bearing MST contain IC consisting predominantly of immunoglobulin. An IgM component which was separated, isolated and identified within IC containing serum displays anti-F(ab')2 reactivity.
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PMID:Immune complexes with antiglobulin activity in sera of Moloney sarcoma-bearing rats. 697 50

Brown Norway (BN) rats were implanted twice with allogeneic (Lewis strain) Moloney sarcoma tumors (LM-2) and serum samples were assessed for Raji binding activity during primary and secondary tumor growth and rejection. Maximum Raji binding was observed 25 days after a primary tumor implant; thereafter, the binding activity decreased. Accelerated tumor rejection was observed after a second tumor implant and was associated with a 3-fold increase in serum Raji binding activity which remained elevated up to 40 days post-tumor implant. Raji binding activity in hyperimmune rats co-migrated with IgG in G-200 fractionated serum. Polyacrylamide gel electrophoresis (PAGE) revealed the presence of bovine serum albumin (BSA) on Raji cell membranes which reacted immunochemically with rabbit anti-BSA antiserum. Immunodiffusion studies revealed that sera from hyperimmune rats produced a precipitin band when reacted with Noniodet P-40 (NP-40) lysates of Raji cells and formed a line of identity with BSA.
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PMID:Detection of Raji binding activity in hyperimmune allogeneic tumor bearing sera associated with anti-BSA activity. 698 Jan 87

Circulating immune complexes (CIC) were quantitated by a Raji cell radioimmunoassay in sera from Brown Norway rats bearing progressing or regressing methylcholanthrene-induced sarcomas. Quantitative profiles of CIC over time were related to tumor dose, tumor mass, and the regressive or progressive course of tumor growth. Animals bearing progressing tumors demonstrated an initial peak of CIC levels by 7 weeks but thereafter displayed a persistent decline in quantities of CIC despite continued tumor growth. Animals bearing regressing tumors were found to have a more directly proportional relationship between the tumor mass and the levels of CIC, but the appearance and disappearance of CIC lagged slightly behind the appearance and disappearance of the tumor. These data are almost identical to data previously published detailing quantities of CIC in BN and Lewis rats bearing Moloney sarcomas and are similar to fluctuations in CIC observed in animals and humans hosting a number of disparate neoplasms.
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PMID:Consistent fluctuations in quantities of circulating immune complexes during progressive and regressive phases of tumor growth. 740 17