Literature DB >> 6297784

Transforming capacities of avian erythroblastosis virus mutants deleted in the erbA or erbB oncogenes.

L Frykberg, S Palmieri, H Beug, T Graf, M J Hayman, B Vennström.   

Abstract

Mutants of avian erythroblastosis virus (AEV) were constructed by deleting large nucleotide segments in each of the viral oncogenes termed v-erbA and v-erbB. Mutants in erbA (erbA -B +) retained the ability to transform fibroblasts in vitro, and these cells exhibited most of the transformation characteristics that typify wild-type AEV-transformed fibroblasts. In addition, the mutants induced small erythroid colonies upon infection of bone marrow cells in culture. Chickens inoculated with erbA -B + virus or with erbA -B +-transformed cells developed sarcomas or atypical erythroid leukemias. The erythroid cells transformed in vivo or in vitro by the erbA -B + viruses appeared not to be as tightly blocked in differentiation as wild-type transformed cells. In contrast, fibroblasts infected with the erbA +B - mutant resembled normal cells in all transformation parameters tested, and no bone marrow cell transformation was observed with the mutant. The results indicate that the main transforming properties of AEV are encoded in erbB and that its effects are enhanced by erbA.

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Year:  1983        PMID: 6297784     DOI: 10.1016/0092-8674(83)90513-5

Source DB:  PubMed          Journal:  Cell        ISSN: 0092-8674            Impact factor:   41.582


  81 in total

1.  Dissecting the activating mutations in v-erbB of avian erythroblastosis virus strain R.

Authors:  H K Shu; R J Pelley; H J Kung
Journal:  J Virol       Date:  1991-11       Impact factor: 5.103

2.  The amino-terminal 14 amino acids of v-src can functionally replace the extracellular and transmembrane domains of v-erbB.

Authors:  M McMahon; R C Schatzman; J M Bishop
Journal:  Mol Cell Biol       Date:  1991-09       Impact factor: 4.272

3.  Ontogeny of the v-erbA oncoprotein from the thyroid hormone receptor: an alteration in the DNA binding domain plays a role crucial for v-erbA function.

Authors:  B G Bonde; M Sharif; M L Privalsky
Journal:  J Virol       Date:  1991-04       Impact factor: 5.103

4.  The lack of transcriptional activation of the v-erbA oncogene is in part due to a mutation present in the DNA binding domain of the protein.

Authors:  H de Verneuil; D Metzger
Journal:  Nucleic Acids Res       Date:  1990-08-11       Impact factor: 16.971

5.  A subpopulation of the avian erythroblastosis virus v-erbA protein, a member of the nuclear hormone receptor family, is glycosylated.

Authors:  M L Privalsky
Journal:  J Virol       Date:  1990-01       Impact factor: 5.103

6.  Sequence-specific DNA binding by the v-erbA oncogene protein of avian erythroblastosis virus.

Authors:  B G Bonde; M L Privalsky
Journal:  J Virol       Date:  1990-03       Impact factor: 5.103

7.  Association of v-ErbA with Smad4 disrupts TGF-beta signaling.

Authors:  Richard A Erickson; Xuedong Liu
Journal:  Mol Biol Cell       Date:  2009-01-14       Impact factor: 4.138

8.  Avian carcinoma virus MH2 contains a transformation-specific sequence, mht, and shares the myc sequence with MC29, CMII, and OK10 viruses.

Authors:  N C Kan; C S Flordellis; C F Garon; P H Duesberg; T S Papas
Journal:  Proc Natl Acad Sci U S A       Date:  1983-11       Impact factor: 11.205

9.  Nucleotide sequence of avian carcinoma virus MH2: two potential onc genes, one related to avian virus MC29 and the other related to murine sarcoma virus 3611.

Authors:  N C Kan; C S Flordellis; G E Mark; P H Duesberg; T S Papas
Journal:  Proc Natl Acad Sci U S A       Date:  1984-05       Impact factor: 11.205

10.  Cellular homologs of the avian erythroblastosis virus erb-A and erb-B genes are syntenic in mouse but asyntenic in man.

Authors:  B U Zabel; R E Fournier; P A Lalley; S L Naylor; A Y Sakaguchi
Journal:  Proc Natl Acad Sci U S A       Date:  1984-08       Impact factor: 11.205

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