Dendritic cell progenitor is transformed by a conditional v-Rel estrogen receptor fusion protein v-ReIER

Boehmelt, Guido; Madruga, Jaime; Ddrfler, Petra; Briegel, Karoline J.; Schwarz, Heinz; Enrietto, Paula J.; Zenke, Martin

doi:10.1016/0092-8674(95)90417-4

Cited by 58 publications

(27 citation statements)

References 41 publications

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“…Moreover, vRel-transformed cell lines, established by in vitro infection of chicken spleen cells and which do not shed helper virus, can induce fatal tumors with as few as 100 cells when injected into histocompatible chickens (Lewis et al, 1981). Cells transformed in vitro by v-Rel have been reported to have characteristics of immature pre-B/pre-T cells (Beug et al, 1981;Chen et al, 1988;Morrison et al, 1991;Zhang et al, 1989), abnormal B cells (Chen et al, 1988), immature and mature B cells (Benatar et al, 1991(Benatar et al, , 1992Boehmelt et al, 1995;Keller et al, 1979;Lewis et al, 1981;Sasaki and Koyama, 1989;Shibuya et al, 1982;Zhang et al, 1991), T cells (Barth et al, 1990;Marmor et al, 1993;Schat et al, 1992), myeloid cells (Barth et al, 1990;Morrison et al, 1991), erythroid cells (Morrison et al, 1991), and pre-dendritic cells (Boehmelt et al, 1995).…”

Section: V-rel As a Member Of The Rel/nf-kb Family Of Transcription Fmentioning

confidence: 99%

Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel

1999

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The avian Rev-T retrovirus encodes the v-Rel oncoprotein, which is a member of the Rel/NF-kB transcription factor family. v-Rel induces a rapidly fatal lymphoma/ leukemia in young birds, and v-Rel can transform and immortalize a variety of avian cell types in vitro. Although Rel/NF-kB transcription factors have been associated with oncogenesis in mammals, v-Rel is the only member of this family that is frankly oncogenic in animal model systems. The potent oncogenicity of v-Rel is the consequence of a number of mutations that have altered its activity and regulation: for example, certain mutations decrease its ability to be regulated by IkBa, change its DNA-binding site speci®city, and endow it with new transactivation properties. The study of v-Rel will continue to increase our knowledge of how cellular Rel proteins contribute to oncogenesis by a ecting cell growth, altering cell-cycle regulation, and blocking apoptosis. This review will discuss biological and molecular activities of v-Rel, with particular attention to how these activities relate to structure ± function aspects of the Rel/NF-kB transcription factors.

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Section: V-rel As a Member Of The Rel/nf-kb Family Of Transcription Fmentioning

confidence: 99%

Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel

1999

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“…c-Myb, a sequence-speci®c DNA-binding protein, is thought to regulate genes whose expression is incompatible with cellular di erentiation as re¯ected in its expression pattern and biological properties (Graf, 1992). Surprisingly, we found that c-myb mRNA increased upon estrogen withdrawal, conditions under which v-RelER cells begin to di erentiate into dendritic and neutrophilic cells (Boehmelt et al, 1995).…”

Section: Expression Of DI Erentially Regulated Genes In V-reler Cellsmentioning

confidence: 59%

Characterization of changes in gene expression associated with malignant transformation by the NF-κB family member, v-Rel

1997

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“…Despite this considerable heterogeneity, several authors have shown that monocytes/macrophages and dendritic cells derive from a common pluripotential haematopoietic progenitor cell in the bone marrow [6,7,[9][10][11][12]. Under appropriate conditions, monocytes/macrophages and dendritic cells can also develop from CD34 + blood stem cells [13,14].…”

Section: A Question Of Paternitymentioning

confidence: 99%

The mononuclear phagocyte–dendritic cell dichotomy: myths, facts, and a revised concept

Goerdt

Kodelja

Schmuth

et al. 1996

Clinical and Experimental Immunology

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SUMMARYSince Aschoff 's reticuloendothelial system was abandoned a few decades ago, classification and characterization of the mononuclear phagocyte and dendritic cell systems have evolved separately or even in competition with one another. New information has now become available indicating that monocytes/macrophages and dendritic cells have a common origin in the bone marrow, and may even transdifferentiate. Morphological and functional distinctions-although valid under certain conditions-have been blurred by revelation of the versatility of monocytes/macrophages and dendritic cells in response to different contextual needs in inflammation and immunity. Monocytes/macrophages and dendritic cells share a sentinel, receptor/effector, and presentation mode, and may either activate or silence specific immune reactions. In keeping with the view of monocytes/macrophages and dendritic cells as interactive sentinels, we suggest that the mononuclear phagocyte and dendritic cell systems be replaced by the custocyte system (custos, Lat sentinel, guard) as a unifying concept. Within the custocyte system, we recognize type I, type II, and type III custocytes. Type I and II custocytes exhibit predominance of presentation or effector/presenter interdependency, respectively, while type III custocytes are bipolar, passing through type I-and type II-like phases during their development and in inflammatory responses. The custocyte system brings into view monocytes/macrophages and dendritic cells as dynamic players in immunity and inflammation with a high degree of derivational, phenotypic, functional, and molecular plasticity.

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Dendritic cell progenitor is transformed by a conditional v-Rel estrogen receptor fusion protein v-ReIER

Cited by 58 publications

References 41 publications

Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel

Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel

Characterization of changes in gene expression associated with malignant transformation by the NF-κB family member, v-Rel

The mononuclear phagocyte–dendritic cell dichotomy: myths, facts, and a revised concept

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