Fusion of the nuclear oncoproteins v-Myb and v-Ets is required for the leukemogenicity of E26 virus
Identifieur interne : 004934 ( Main/Exploration ); précédent : 004933; suivant : 004935Fusion of the nuclear oncoproteins v-Myb and v-Ets is required for the leukemogenicity of E26 virus
Auteurs : Thomas Metz [Allemagne] ; Thomas Graf [Allemagne]Source :
- Cell [ 0092-8674 ] ; 1991.
English descriptors
- Teeft :
- Amino, Amino acids, Assay, Avian, Beug, Blastoderm, Blastoderm medium, Blastoderm transformation assay, Bone marrow, Breakpoints, Cause leukemia, Cell surface antigens, Chicken embryos, Codon, Deletion, Deletion breakpoints, Embryo, Encode, Eosinophilic lineages, Erythroblastosis, Erythroid, Erythroid cells, Fusion, Fusion protein, Fusion proteins, Genome, Genomic, Graf, Latency, Leukemia, Leukemia induction, Leukemic, Leukemic animals, Leukemic cells, Leukemogenic, Leukemogenic variants, Leukemogenicity, Long terminal, Metz, Moscovici, Myblets, Myblets viruses, Myeloid, Myeloid cells, Nonleukemic animal, Novel fusion proteins, Nuclear oncogenes, Nucleotide, Oncogene, Oncoproteins, Parental, Parental myblets viruses, Parental virus, Parental viruses, Primer, Protein, Proviral genomes, Results show, Retrovirus, Right mark, Separate proteins, Transactivation, Transactivation domain, Transcriptional, Translocation, Unpublished data, Variant, Variant viruses, Viral, Viral genome, Virus.
Abstract
Abstract: The highly leukemogenic avian retrovirus E26 expresses the two transcriptional activator-type oncogenes v-myb and v-ets as a nuclear fusion protein. Previous studies have shown that both oncogenes cooperate in the transformation of erythroid cells in vitro and that the phenotypes of transformed cells differ, depending on whether the oncogenes are coexpressed as separate proteins or as a fusion protein. Here we show that virus constructs encoding either v-Myb or v-Ets as their only oncoprotein are nonleukemogenic and that constructs coexpressing nonfused v-Myb and v-Ets proteins appear to be weakly leukemogenic. Surprisingly, leukemic animals injected with the latter contain highly leukemogenic variant viruses that exhibit internal deletions in their genome, resulting in the synthesis of novel Myb-Ets fusion proteins. These results show that v-Myb and v-Ets must be fused to cause leukemia and establish a new mechanism of oncogene activation and cooperation.
Url:
DOI: 10.1016/0092-8674(91)90142-L
Affiliations:
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Fusion of the nuclear oncoproteins v-Myb and v-Ets is required for the leukemogenicity of E26 virus</title><author><name sortKey="Metz, Thomas" sort="Metz, Thomas" uniqKey="Metz T" first="Thomas" last="Metz">Thomas Metz</name></author><author><name sortKey="Graf, Thomas" sort="Graf, Thomas" uniqKey="Graf T" first="Thomas" last="Graf">Thomas Graf</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:4EA55FDBE6A6EB2E26516E895EA6A914AC2025A9</idno><date when="1991" year="1991">1991</date><idno type="doi">10.1016/0092-8674(91)90142-L</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-R30VW65F-8/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">002556</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002556</idno><idno type="wicri:Area/Istex/Curation">002556</idno><idno type="wicri:Area/Istex/Checkpoint">001E77</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">001E77</idno><idno type="wicri:doubleKey">0092-8674:1991:Metz T:fusion:of:the</idno><idno type="wicri:Area/Main/Merge">004A10</idno><idno type="wicri:Area/Main/Curation">004934</idno><idno type="wicri:Area/Main/Exploration">004934</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Fusion of the nuclear oncoproteins v-Myb and v-Ets is required for the leukemogenicity of E26 virus</title><author><name sortKey="Metz, Thomas" sort="Metz, Thomas" uniqKey="Metz T" first="Thomas" last="Metz">Thomas Metz</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Differentiation Programme European Molecular Biology Laboratory 6900 Heidelberg</wicri:regionArea></affiliation></author><author><name sortKey="Graf, Thomas" sort="Graf, Thomas" uniqKey="Graf T" first="Thomas" last="Graf">Thomas Graf</name><affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Differentiation Programme European Molecular Biology Laboratory 6900 Heidelberg</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Cell</title><title level="j" type="abbrev">CELL</title><idno type="ISSN">0092-8674</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">66</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="95">95</biblScope><biblScope unit="page" to="105">105</biblScope></imprint><idno type="ISSN">0092-8674</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0092-8674</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Amino</term><term>Amino acids</term><term>Assay</term><term>Avian</term><term>Beug</term><term>Blastoderm</term><term>Blastoderm medium</term><term>Blastoderm transformation assay</term><term>Bone marrow</term><term>Breakpoints</term><term>Cause leukemia</term><term>Cell surface antigens</term><term>Chicken embryos</term><term>Codon</term><term>Deletion</term><term>Deletion breakpoints</term><term>Embryo</term><term>Encode</term><term>Eosinophilic lineages</term><term>Erythroblastosis</term><term>Erythroid</term><term>Erythroid cells</term><term>Fusion</term><term>Fusion protein</term><term>Fusion proteins</term><term>Genome</term><term>Genomic</term><term>Graf</term><term>Latency</term><term>Leukemia</term><term>Leukemia induction</term><term>Leukemic</term><term>Leukemic animals</term><term>Leukemic cells</term><term>Leukemogenic</term><term>Leukemogenic variants</term><term>Leukemogenicity</term><term>Long terminal</term><term>Metz</term><term>Moscovici</term><term>Myblets</term><term>Myblets viruses</term><term>Myeloid</term><term>Myeloid cells</term><term>Nonleukemic animal</term><term>Novel fusion proteins</term><term>Nuclear oncogenes</term><term>Nucleotide</term><term>Oncogene</term><term>Oncoproteins</term><term>Parental</term><term>Parental myblets viruses</term><term>Parental virus</term><term>Parental viruses</term><term>Primer</term><term>Protein</term><term>Proviral genomes</term><term>Results show</term><term>Retrovirus</term><term>Right mark</term><term>Separate proteins</term><term>Transactivation</term><term>Transactivation domain</term><term>Transcriptional</term><term>Translocation</term><term>Unpublished data</term><term>Variant</term><term>Variant viruses</term><term>Viral</term><term>Viral genome</term><term>Virus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The highly leukemogenic avian retrovirus E26 expresses the two transcriptional activator-type oncogenes v-myb and v-ets as a nuclear fusion protein. Previous studies have shown that both oncogenes cooperate in the transformation of erythroid cells in vitro and that the phenotypes of transformed cells differ, depending on whether the oncogenes are coexpressed as separate proteins or as a fusion protein. Here we show that virus constructs encoding either v-Myb or v-Ets as their only oncoprotein are nonleukemogenic and that constructs coexpressing nonfused v-Myb and v-Ets proteins appear to be weakly leukemogenic. Surprisingly, leukemic animals injected with the latter contain highly leukemogenic variant viruses that exhibit internal deletions in their genome, resulting in the synthesis of novel Myb-Ets fusion proteins. These results show that v-Myb and v-Ets must be fused to cause leukemia and establish a new mechanism of oncogene activation and cooperation.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Metz, Thomas" sort="Metz, Thomas" uniqKey="Metz T" first="Thomas" last="Metz">Thomas Metz</name></noRegion><name sortKey="Graf, Thomas" sort="Graf, Thomas" uniqKey="Graf T" first="Thomas" last="Graf">Thomas Graf</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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