Structure and expression of c-rel, the cellular homolog to the oncogene of reticuloendotheliosis virus strain T

Chen, I. S Y; Wilhelmsen, K. C.; Temin, Howard M.

doi:10.1128/jvi.45.1.104-113.1983

Cited by 57 publications

(16 citation statements)

References 29 publications

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“…Immunological reagents. Antisera specific for the carboxy terminus, amino terminus, and midregion of the v-rel protein have been previously described (8,26). Antiserum directed against full-length v-rel protein expressed in plasmid pOTS in Escherichia coli is described by Lim et al (submitted).…”

Section: Methodsmentioning

confidence: 99%

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Avian reticuloendotheliosis virus-transformed lymphoid cells contain multiple pp59v-rel complexes

Davis

Bargmann

Lim

et al. 1990

J Virol

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The v-rel oncogene of avian reticuloendotheliosis virus type T (REV-T) encodes a 59-kilodalton (kDa) phosphoprotein located principally in the cytosol of transformed lymphoid cells. All of the detectable pp59v-rel was present in high-molecular-weight complexes containing at least five cellular proteins (p124, p115, p75c-rel p70hsC, and pp4O). Antiserum was developed against the 40-kDa protein, the most abundant cellular protein associated with the complex. The 40-kDa phosphoprotein was complexed with pp59v-rel in REV-T-transformed lymphoid cell lines arrested at different stages of B-cell development as well as in lymphoid tumor cells and in fibrosarcomas. The half-life (8 h) of pp4O in REV-T-transformed lymphoid cells was the same as that of pp59v-rel. Antiserum against pp4O permitted the identification of two pp59v-rel complexes. The most abundant cytoplasmic complex contained approximately 75% of the pp59v-rel and all of the detectable pp4O in REV-T-transformed lymphoid cells. Twenty-five percent of the pp59v-rel was present in a minor complex that contained the majority of p75crel along with p115 and p124. In nuclear extracts of REV-T-transformed lymphoid cells, pp59v-re was complexed with pp4O. The two high-molecular-weight proteins (p115 and p124) and p75c're were not detected in the nuclear complex. In the cytosolic complexes, pp4O was heavily phosphorylated, whereas the nuclear form was much less extensively phosphorylated.

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Section: Methodsmentioning

confidence: 99%

“…This 1.4-kilobase sequence, designated v-rel, is inserted within envelope sequences at the 3' end of the virus genome (7,27). The v-rel oncogene is distinct from other known oncogenes (7,8,39) and is transcribed into a 3.0-kilobase subgenomic RNA that is found at modest levels in REV-T-transformed lymphoid cells (8,17).…”

mentioning

confidence: 99%

Avian reticuloendotheliosis virus-transformed lymphoid cells contain multiple pp59v-rel complexes

Davis

Bargmann

Lim

et al. 1990

J Virol

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“…A turning point came from the study of oncogenic viruses, especially from the Retroviridae family which led to a "shocking" discovery. These viruses induced cancer through the expression of oncogenes, which had their corresponding cellular variants [39][40][41][42][43][44][45][46][47]. These oncogenes included v-raf, c-my, c-rel, and k-ras among others.…”

Section: Tumour Antigenicitymentioning

confidence: 99%

Tumour Immunogenicity, Antigen Presentation, and Immunological Barriers in Cancer Immunotherapy

Escors

2014

New Journal of Science

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Since the beginning of the 20th century, scientists have tried to stimulate the antitumour activities of the immune system to fight against cancer. However, the scientific effort devoted on the development of cancer immunotherapy has not been translated into the expected clinical success. On the contrary, classical antineoplastic treatments such as surgery, radiotherapy, and chemotherapy are the first line of treatment. Nevertheless, there is compelling evidence on the immunogenicity of cancer cells and the capacity of the immune system to expand cancer-specific effector cytotoxic T cells. However, the effective activation of anticancer T cell responses strongly depends on efficient tumour antigen presentation from professional antigen presenting cells such as dendritic cells (DCs). Several strategies have been used to boost DC antigen presenting functions, but at the end cancer immunotherapy is not as effective as would be expected according to preclinical models. In this review, we comment on these discrepancies, focusing our attention on the contribution of regulatory T cells and myeloid-derived suppressor cells to the lack of therapeutic success of DC-based cancer immunotherapy.

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“…We have previously determined that c-rel is transcribed at low levels in many tissues. Analysis of c-rel mRNA from chicken spleen cells indicates that more of the c-rel locus is transcribed than the sequences of c-rel that are homologous to v-rel (5).…”

Section: Rev-mentioning

confidence: 99%

Nucleic acid sequences of the oncogene v-rel in reticuloendotheliosis virus strain T and its cellular homolog, the proto-oncogene c-rel

Wilhelmsen¹,

Eggleton²,

Temin³

1984

J Virol

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275

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Reticuloendotheliosis virus strain T (Rev-T) is a highly oncogenic replication-defective retrovirus which contains the oncogene v-rel. It is thought that Rev-T arose when a virus similar to Rev-A, the helper virus of Rev-T, infected a turkey and recombined with c-rel from that turkey. There is one large c-rel locus in the turkey genome which contains all of the sequences homologous to v-rel (K. C. Wilhelmsen and H. M. Temin, J. Virol. 49:521-529, 1984). We have sequenced v-rel and its flanking sequences, each of the regions of the c-rel locus from turkey that are homologous to v-rel and their flanking sequences, and the coding sequence for env and part of pol of Rev-A. The v-rel coding sequences can be translated into a 503-amino acid env-v-rel-out-offrame-env fusion polypeptide. We have not detected any sequences in the Los Alamos or University of California-San Diego data bases that are more significantly related to the amino acid or nucleic acid sequence of v-rel than to the randomized sequence of v-rel. Comparison of Rev-A, Rev-T, and c-rel indicates that the v-rel sequences may have been transduced from the c-rel (turkey) locus by a novel mechanism. There are sequences in Rev-A and c-rel that are similar to splicing signals, indicating that the 5' virus-rel junction of Rev-T may have been formed by cellular RNA splicing machinery. Eight presumed introns have presumably been spliced out of c-rel to generate v-rel. There are also short imperfect regions of homology between sequences at the boundaries of v-rel and sequences in Rev-A and c-rel (turkey), indicating that c-rel may have been transduced by homologous recombination. There are many differences between the amino acid sequences of the predicted translational products of v-rel and c-rel which may account for their difference in transformation potential. These sequence differences between v-rel and c-rel include 10 missense transitions, four missense transversions, and three places where Rev-T has a small in-frame deletion of sequences relative to c-rel. Most of the coding sequence differences between c-rel and v-rel are nonconservative amino acid changes. * Corresponding author. 172 gene appears to be the result of a quantitative difference in the level of their expression (13, 30). We have been studying the highly oncogenic retrovirus reticuloendotheliosis virus strain T (Rev-T), which contains the oncogene v-rel. Rev-T was first isolated from a turkey (28). It is thought that Rev-T arose when a virus similar to Rev-A infected a turkey and recombined with c-rel from that turkey. Analysis of molecular clones of proviruses of Rev-T and Rev-A (Rev-A is the nondefective helper virus of Rev-T) shows that in Rev-T, v-rel is substituted for most of env in Rev-A (see Fig. 1) (3, 8, 18). Rev-T also has a large deletion of sequences which encode much of gag and pol in Rev-A. This deletion is necessary for transformation of cells by v-rel (4). In Rev-T-infected cells, there are two viral RNA transcripts that contain v-rel sequences: a full-length genomic size tran...

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Structure and expression of c-rel, the cellular homolog to the oncogene of reticuloendotheliosis virus strain T

Cited by 57 publications

References 29 publications

Avian reticuloendotheliosis virus-transformed lymphoid cells contain multiple pp59v-rel complexes

Avian reticuloendotheliosis virus-transformed lymphoid cells contain multiple pp59v-rel complexes

Tumour Immunogenicity, Antigen Presentation, and Immunological Barriers in Cancer Immunotherapy

Nucleic acid sequences of the oncogene v-rel in reticuloendotheliosis virus strain T and its cellular homolog, the proto-oncogene c-rel

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