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

Davis, Nathan; Bargmann, William; Lim, Moon Young; Bose, Henry R.

doi:10.1128/jvi.64.2.584-591.1990

Cited by 61 publications

(24 citation statements)

References 39 publications

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“…The results indicate that IB-␣ expressed alone in these cells has a short half-life (1 to 2 h). In DT95 cells expressing v-Rel, the v-Rel in the transformed cells is complexed with IB-␣ (data not shown), as previously reported for other lymphoid cells lines and avian fibroblasts (21,22,67). In the cells expressing c-Rel or v-Rel, the half-life of IB-␣ corresponded to the half-life of the associated Rel protein (about 12 h in DT95 cells expressing c-Rel and IB-␣ and approximately 8 h in DT95 cells expressing v-Rel and IB-␣).…”

Section: Kinetic Analysis Of Ikba Nfkb1 and Mhc Class II Expressionsupporting

confidence: 84%

“…These results suggest that IB-␣ is stabilized through an association with Rel proteins, in a manner similar to that described for RelA (81). This possibility is also supported by the observation that the half-life of IB-␣ and v-Rel in a v-Rel-transformed cell line is the same (approximately 7 h) (21). To test this hypothesis directly, the half-life of IB-␣ was measured 4 days after infection of DT95 cells infected with a retrovirus expressing IB-␣ and either c-Rel or v-Rel (Fig.…”

Section: Kinetic Analysis Of Ikba Nfkb1 and Mhc Class II Expressionsupporting

confidence: 76%

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The relocalization of v-Rel from the nucleus to the cytoplasm coincides with induction of expression of Ikba and nfkb1 and stabilization of I kappa B-alpha

Hrdličková

Nehyba

Roy

et al. 1995

J Virol

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The v-Rel oncogene induces the expression of major histocompatibility complex class I and II proteins and the interleukin-2 receptor more efficiently than does c-Rel (R. Hrdličková, J. Nehyba, and E. H. Humphries, J. Virol. 68:308-319, 1994). The kinetics with which these immunoregulatory receptors are induced in B-and T-lymphoid cell lines and chicken embryo fibroblast cultures expressing c-Rel or v-Rel have been examined. v-Rel induced the expression of major histocompatibility complex classes I and II and interleukin-2 receptor more efficiently than did c-Rel at later times after infection. In all three cell types, this increased efficiency was accompanied by a shift in the majority of v-Rel from the nucleus to the cytoplasm. The concomitant relocalization of v-Rel was also demonstrated during the in vitro transformation of spleen cells. The translocation coincided with increased steady-state levels of IB-␣. Coinfection by retroviral vectors expressing v-Rel, IB-␣, or NF-B1 demonstrated that either IB-␣ or NF-B1 can contribute to the shift of v-Rel to the cytoplasmic compartment. The induction of nfkb1and Ikba mRNA and the stabilization of IB-␣ by v-Rel were shown to be responsible for these effects. In comparison with c-Rel, the expression of v-Rel was associated with lower levels of transcription of these genes. However, the ability of v-Rel to stabilize IB-␣ remained unchanged. The ability of v-Rel to stabilize IB-␣ but poorly induce Ikba mRNA expression relative to c-Rel may play a role in regulating gene expression, thereby leading to transformation.

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Section: Kinetic Analysis Of Ikba Nfkb1 and Mhc Class II Expressionsupporting

confidence: 84%

Section: Kinetic Analysis Of Ikba Nfkb1 and Mhc Class II Expressionsupporting

confidence: 76%

The relocalization of v-Rel from the nucleus to the cytoplasm coincides with induction of expression of Ikba and nfkb1 and stabilization of I kappa B-alpha

Hrdličková

Nehyba

Roy

et al. 1995

J Virol

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“…The cytoplasmic retention may be due to physical association with other proteins or to posttranslational modifications. Other members of the NF-B inhibitor family have been also observed in the nucleus (4,11,28,45).…”

Section: Discussionmentioning

confidence: 99%

Bcl-3 Expression Promotes Cell Survival following Interleukin-4 Deprivation and Is Controlled by AP1 and AP1-Like Transcription Factors

et al. 2000

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We have analyzed the interleukin-4 (IL-4)-triggered mechanisms implicated in cell survival and show here that IL-4 deprivation induces apoptotic cell death but does not modulate Bcl-2 or Bcl-x expression. Since Bcl-x expression is insufficient to ensure cell survival in the absence of IL-4, we speculate that additional molecules replace the antiapoptotic role of Bcl-2 and Bcl-x in an alternative IL-4-triggered pathway. Cell death is associated with Bcl-3 downregulation and Bcl-3 expression blocks IL-4 deprivation-induced apoptosis, suggesting that Bcl-3 acts as a survival factor in the absence of growth factor. To characterize the IL-4-induced regulation of murine Bcl-3 expression, we cloned the promoter of this gene. Sequencing of the promoter showed no TATA box element but did reveal binding sites for AP1, AP1-like, and SP1 transcription factors. Retardation gels showed that IL-4 specifically induces AP1 and AP1-like binding activity and that mutation of these binding sites abolishes the IL-4-induced Bcl-3 promoter activity, suggesting that these transcription factors are important in Bcl-3 promoter transactivation. IL-4 deprivation induces downregulation of Jun expression and upregulation of Fos expression, both of which are proteins involved in the formation of AP1 and AP1-like transcription factors. Overexpression of Jun family proteins transactivates the promoter and restores Bcl-3 expression in the absence of IL-4 stimulation. Taken together, these data describe a new biological role for Bcl-3 and define the regulatory pathway implicated in Bcl-3 expression.

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“…The potential KB binding site of chicken MHC class I gene promoter referred to as the class I-responsive element was shifted in an electrophoretic mobility assay with a v-rel-estrogen receptor fusion protein (13). The majority of v-rel protein is localized in the cytoplasmic compartment of transformed lines; however, significant levels can be detected in the nucleus (29,59,78). For these reasons, both direct and indirect mechanisms can effect v-relmediated gene expression.…”

Section: Discussionmentioning

confidence: 99%

“…The transactivation capability of v-rel indicates that it can induce the expression of MHC class I, MHC class II, and IL-2R proteins by direct interaction with DNA KB sites (34,40,66,77). On the other hand, the presence of a majority of v-rel protein in cytoplasmic complexes with IKBoX, NFKB1, NFKB2, and c-rel suggests that an indirect mechanism may also contribute to the v-rel-mediated induction of gene expression (17,29,30,70).…”

Section: Discussionmentioning

confidence: 99%

v-rel induces expression of three avian immunoregulatory surface receptors more efficiently than c-rel

Hrdličková

Nehyba

Humphries

1994

J Virol

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The c-rel gene is a member of NF-KBIrel family of transcription factors that regulate expression of a variety of immunoregulatory molecules. The virat oncogene, v-rel, is a truncated and mutated form of the turkey c-rel gene expressed by reticuloendotheliosis virus, strain T. In this study, we demonstrated that three avian immunoregulatory receptors, major histocompatibility (MHC) antigens class I and class II as well as the interleukin-2 receptor (IL-2R), were induced on the surface of splenic tumor cells isolated from chickens infected with reticuloendotheliosis virus, strain T. All cell lines derived from splenic tumors expressed these three proteins. Their expression also correlated with the appearance of endogenous c-rel during a graft-versushost reaction. In vitro, both c-rel and v-rel induced MHC class I, MHC class II, and IL-2R on an avian B-lymphoid cell line, DT95, and a T-lymphoid cell line, MSB-1. Quantitative kinetic analysis demonstrated both the accumulation of MHC class II mRNA and the appearance of surface MHC class II protein in response to the synthesis of either v-rel or c-rel. We show that v-rel induced the expression of MHC class II in the avian B-cell lines DT40 and DT95 more rapidly than c-rel and that, several weeks after infection, v-rel induced MHC class II as much as 50-fold more efficiently than c-rel. Finally, in vitro infection of splenocytes with retroviruses that express v-rel or c-rel induced MHC class I, MHC class II, and IL-2R expression. Quantitative analysis confirmed that p59v-re was consistently more efficient at inducing expression of all three immunoregulatory receptors than exogenous p68c-er. These data suggest that during tumor development, v-rel functions to induce (or suppress) the expression of genes similarly induced (or suppressed) by c-rel. The observations reported in this study are not in agreement with a model in which v-rel promotes tumor development by functioning as a dominant negative mutant of c-rel. In contrast, these findings support the hypothesis that lymphocyte immortalization and tumor development are the result, at least in part, of the capacity of v-rel to function as a dominant positive mutant that induces expression of genes normally regulated by c-rel.

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

Cited by 61 publications

References 39 publications

The relocalization of v-Rel from the nucleus to the cytoplasm coincides with induction of expression of Ikba and nfkb1 and stabilization of I kappa B-alpha

The relocalization of v-Rel from the nucleus to the cytoplasm coincides with induction of expression of Ikba and nfkb1 and stabilization of I kappa B-alpha

Bcl-3 Expression Promotes Cell Survival following Interleukin-4 Deprivation and Is Controlled by AP1 and AP1-Like Transcription Factors

v-rel induces expression of three avian immunoregulatory surface receptors more efficiently than c-rel

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