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)

A new chromatographic material based on beads of macroporous crosslinked agarose containing ferric oxide particles was used for enrichment of gp70--the envelope glycoprotein of feline leukemia virus (FeLV). Free gp70 was purified from cell culture fluid in one step with a recovery of 50 to 60% and a purification of about 60 times. The described procedure is a suitable first step for the purification of gp70 from large volumes of cell culture fluid.
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PMID:Free gp70 from FeLV: enrichment from cell culture fluid by ferric oxide-agarose chromatography. 254 38

The gp52 envelope glycoprotein of Friend spleen focus-forming virus (SFFV) is a recombinant molecule derived from Friend murine leukemia virus (MuLV) by various deletions, insertions, and substitutions. The SFFV gp52 glycoprotein, unlike MuLV envelope glycoproteins, is defective in transport to the cell surface. Only 3-5% of gp52 eventually reaches the cell surface as a processed form (gp65). Although gp52 lacks cytoplasmic tail residues found in MuLV glycoproteins, we have previously shown that this deletion is not responsible for its defective transport. In order to investigate the basis for the defective transport of gp52, we have examined the folding and assembly of gp52 molecules into oligomeric molecules. CV-1 cells infected with vaccinia virus recombinants expressing SFFV gp52 were pulse labeled and the cell extracts were fractionated by velocity centrifugation through sucrose gradients. Immediately after a 10-min pulse, gp52 was detected as a monomer in the upper part of the sucrose gradient (fractions 12 and 14) and it remained as such after a 2-h chase period. However, the processed form, gp65, was found in a lower part of the gradient (fraction 8) after a 2-h chase. The position of gp65 was found to correspond to the position of trimeric influenza hemagglutinin which was analyzed on a parallel sucrose gradient, suggesting that gp65 also exists as a trimer in this fraction. These results indicate that changes in the external domain of gp52 result in improper folding of the glycoprotein molecule, and suggest that this lack of oligomerization is responsible for the defective transport of the molecules. Only those molecules that do form oligomeric structures are transported to the Golgi complex and undergo further oligosaccharide processing, and transport to the cell surface.
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PMID:The spleen focus-forming virus envelope glycoprotein is defective in oligomerization. 254 80

The complete nucleotide sequence of two human T-cell leukaemia type III (HTLV-III) proviral DNAs each have four long open reading frames, the first two corresponding to the gag and pol genes. The fourth open reading frame encodes two functional polypeptides, a large precursor of the major envelope glycoprotein and a smaller protein derived from the 3'-terminus long open reading frame analogous to the long open reading frame (lor) product of HTLV-I and -II.
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PMID:Complete nucleotide sequence of the AIDS virus, HTLV-III. 257 15

The envelope glycoproteins of the human immunodeficiency virus (HIV) type 1 are synthesized as a precursor molecule, gp160, which is cleaved to generate the two mature envelope glycoproteins, gp120 and gp41. The cleavage reaction, which is mediated by a host protease, occurs at a sequence highly conserved in retroviral envelope glycoprotein precursors. We have investigated the sequence requirements for this cleavage reaction by introducing four single-amino-acid changes into the glutamic acid-lysine-arginine sequence immediately amino terminal to the site of cleavage. We have also examined the effects of these mutations on the syncytium formation induced by HIV envelope glycoproteins. Our results indicate that a glutamic acid to glycine change at gp120 amino acid 516, a lysine to isoleucine change at amino acid 517, and an arginine to lysine change at amino acid 518 affect neither gp160 cleavage nor syncytium formation. The results obtained with the arginine to lysine change at amino acid 518 differ significantly from the results obtained with the same mutation at the envelope precursor cleavage site of a murine leukemia virus (E. O. Freed, and R. Risser, J. Virol. 61:2852-2856, 1987). An arginine to threonine mutation at gp120 amino acid 518, the terminal residue of gp120, abolishes both gp160 cleavage and syncytium formation. These findings demonstrate that despite its highly conserved nature, the basic pair of amino acids at the site of gp160 cleavage is not absolutely required for proper envelope glycoprotein processing. This report also supports the idea that cleavage of gp160 is required for activation of the HIV envelope fusion function.
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PMID:Mutational analysis of the cleavage sequence of the human immunodeficiency virus type 1 envelope glycoprotein precursor gp160. 267

The primary protein product of the human T-cell leukemia virus type 1 (HTLV-1) env gene, gp61, is cleaved to produce both the exterior (gp46) and the transmembrane (gp21) portions of the HTLV-1 envelope protein. To compare the reactivity with human antibodies of different regions of this gp61 protein, five plasmids (A, B, B1, C, and D) were constructed to express recombinant proteins (RPs) in Escherichia coli. RP-A, RP-B, RP-B1, and RP-C contain amino acid residues 26 to 165, 166 to 229, 166 to 201, and 229 to 308, respectively, of the exterior envelope protein gp46. Serum samples from HTLV-1-seropositive subjects were assayed for reactivity with these RPs by Western immunoblotting. The percentages of positive reactivity with each of the RPs were as follows: 18.9% (23 of 122) for RP-A, 89.6% (112 of 125) for RP-B, 70.2% (85 of 121) for RP-B1, and 92.9% (117 of 126) for RP-C. These results indicate that the C-terminal half of gp46 (RP-B plus RP-C) can detect 97.6% (123 of 126) of positive samples, while the N-terminal half of gp46 (RP-A) can only detect 18.9% of the HTLV-1-positive sera (P less than 0.005). Furthermore, RP-A, -B, and -C, which together span the entire length of gp46 except the first five amino acids at the N terminus and the last four amino acids at the C- terminus, detected 99.2% (125 of 126) of the HTLV-1-positive subjects. In contrast, RP-D, which contains the HTLV-1 transmembrane envelope protein gp21 minus the first amino acid at the N terminus, had a lower rate of antibody reactivity at 73.7% (84 of 114) (P less than 0.005). The difference in seropositive rates for RP-D between HTLV-1 carriers (55.6%) and adult T-cell leukemia patients (85.5%) is statistically significant (P less than 0.01). This study therefore indicates that the C-terminal half of gp46, especially the amino acid sequence from 200 to 308, contains the most reactive epitopes of the HTLV-1 gp61 envelope glycoprotein.
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PMID:Antibody reactivity to different regions of human T-cell leukemia virus type 1 gp61 in infected people. 267 6

Antibodies against the retrovirus envelope glycoprotein (gp70) of mouse xenotropic retrovirus, BALB virus 2 (Bv2) reacted with the adult worms of Schistosoma japonicum and S. mansoni. This reaction was completely inhibited after adsorption of the antibodies with virions of retrovirus. The reactive schistosome antigen was located in the subtegumental layer of the adult male fluke and in the vitelline gland of the adult female of S. japonicum and S. mansoni. Proteins extracted from both parasites were examined by immunoblot analysis. Anti-Bv2 gp70 antiserum reacted with those proteins from both schistosomes and the band patterns were different among sexes and species. Southern hybridization of the DNA extracted from adults of S. japonicum and S. mansoni demonstrated the presence of sequences homologous to the env gene of mouse ecotropic and xenotropic retroviruses. DNA sequences homologous to the gag and pol regions of the ecotropic murine leukaemia virus were also detected in the DNAs of schistosomes.
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PMID:Integration and expression of murine retrovirus-related sequences in schistosomes. 279 70

The N-terminal segment of human interleukin-2 (hIL-2) appears to mediate binding of the beta hIL-2 receptor (R. Robb, C. Rusk, J. Yodoi, and W. Greene, Proc. Natl. Acad. Sci. USA 84:2002-2006, 1987). An affinity-purified antibody prepared against this peptide segment (p81) is shown here to cross-react with a homologous region of the human T-cell leukemia virus type I (HTLV-I) envelope glycoprotein, raising the interesting possibility that the envelope glycoprotein of HTLV-I can interact with the beta hIL-2 receptor.
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PMID:Immunological and structural homology between human T-cell leukemia virus type I envelope glycoprotein and a region of human interleukin-2 implicated in binding the beta receptor. 282 24

Previous studies in our laboratory and others have been consistent with the hypothesis that the envelope (env) gene of the spleen focus-forming virus (SFFV) is the only gene essential for the induction of acute erythroleukemia. However, no studies have been carried out with the SFFV env gene in the complete absence of other SFFV sequences. To accomplish this goal, we isolated the sequences that encode the envelope glycoprotein, gp52, of SFFVA and expressed them in a Moloney murine leukemia virus-based double-expression vector containing the neomycin resistance gene. The method used to produce retrovirus stocks in tissue culture cells affected the expression of the gp52 gene in the vector and the subsequent pathogenicity of the vector in mice. Highly pathogenic virus stocks were obtained by cotransfection of vector and helper virus DNAs into fibroblasts, followed by virus replication and spread through the cell population. Mice infected with this stock developed a rapid erythroid disease that was indistinguishable from that induced by the entire SFFV genome, and the virus stock transformed erythroid cells in vitro. Spleen cells from the diseased mice expressed the SFFV env gene product but not the SFFV gag gene product. As expected, mice given the virus containing the SFFV env gene in the reverse orientation did not express the SFFV env gene product or develop erythroleukemia. This study, therefore, demonstrated (i) that double-expression retroviral vectors can be used under specific conditions to produce viruses expressing high levels of a particular gene and (ii) that incorporation of the SFFV env gene into such a vector in the absence of other SFFV sequences results in a retrovirus which is as pathogenic as the original SFFV.
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PMID:The spleen focus-forming virus (SFFV) envelope gene, when introduced into mice in the absence of other SFFV genes, induces acute erythroleukemia. 283 16

Multiple copies of retroviral sequences are stably integrated in the genomes of many higher organisms, and are thus transmitted vertically to offspring via the germline (1). Most of these heritable viral genes are not expressed, and expression, when observed, is commonly limited to envelope (env) genes as demonstrated by the presence of cell surface and serum envelope glycoprotein (gp70) in mice. Studies of the mouse have shown that certain tissues such as the reproductive tract and lymphoid organs are common sites for the expression of endogenous env genes, suggesting that the transcription of at least some endogenous sequences is tissue specific. The transcription of endogenous viral genes is regulated by both cis and trans mechanisms (2-5) and their expression can be temporally linked to differentiation and development (6-8). The consequences to the host of endogenous retroviral genes are varied. At one extreme, expression of endogenous virus can result in the development of leukemia and death. Another potentially detrimental effect is that of insertional mutagenesis, seen when the integration of retroviral sequences interrupts the functioning of a cellular gene (9, 10). However, it is now clear that expression of endogenous retroviral genes may also have a beneficial effect for the host: namely, mediating resistance to retroviral leukemias as has been demonstrated for the Fv-4 gene in mice (11) and some ea loci in chickens (12). This form of resistance is due to the blockage of cellular viral receptors by the expression of envelope glycoprotein on the cell surface. The Rmcf locus of the mouse is another resistance gene that may exert its effect by the expression of an endogenous env gene. A summary of our current state of knowledge concerning the Rmcf gene is shown in Table I. The Rmcf gene was originally described when it was observed that fibroblast cell cultures derived from certain strains of mice restricted the replication of recombinant mink cell focus-forming(MCF)1 viruses (13). As detailed in Table I, DBA/2 mice are the prototypic strain exhibiting the Rmcf resistance (Rmcf(r)) phenotype. Cell cultures from other strains, such as C57BL/6 and IRW, are permissive for MCF viral replication and are termed Rmcf sensitive (Rmcf(s)). Previously, we described two allelic forms of an endogenous env gene, whose expression is linked to the Rmcf gene (14). Cell cultures from Rmcf(r) mice express gp70 related to that of MCF viruses, whereas cultures derived from Rmcf(s) mice either express no gp70 (IRW) or express an endogenous xenotropic gp70 (C57BL/6). These two gp70 alleles are detectable by type-specific mAbs.
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PMID:A population of murine hematopoietic progenitors expresses an endogenous retroviral gp70 linked to the Rmcf gene and associated with resistance to erythroleukemia. 292 25

A highly leukemogenic virus (DMBA-LV) (in vivo leukemogenic titer 1-5 X 10(6) IU/ml, and 35-40 days to thymic lymphoma detection) is produced by a chemical carcinogen-induced transplanted thymic lymphoma. The virus preparation is a mixture of a type-B retrovirus highly related to exogenous type-B retroviral isolates and a biologically defective type-C retrovirus. The DNA of DMBA-LV-induced-tumors contains new type-B proviruses but no additional type-C proviruses could be detected. The leukemogenicity of DMBA-LV was completely neutralized by a monoclonal antibody against MMTV envelope glycoprotein, but was not affected by a broadly reacting Friend MuLV anti-gp70 serum which effectively neutralizes type-C ecotropic, xenotropic, and recombinant retroviruses and which completely abolishes the leukemogenic activity of Moloney leukemia virus. Three type-B mammary tumor-inducing retroviral isolates, while containing type-C retroviral sequences, were not leukemogenic. A further characterization of the type-C retroviral sequences present in DMBA-LV indicated that sequences characteristic of endogenous, nonxenotropic proviruses are present. In addition, using a variety of type-C-specific retroviral DNA probes, no evidence was obtained for the presence of a type-B-C-recombinant genome in DMBA-LV. Leukemogenesis was absolutely dependent upon the presence of a functional type-B retroviral envelope gp 52 and DMBA-LV does not appear to contain a leukemogenic retroviral type-C genome.
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PMID:The involvement of a type-B retrovirus in the induction of thymic lymphomas. 298 51


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