Literature DB >> 6297744

Substitution of 5' helper virus sequences into non-rel portion of reticuloendotheliosis virus strain T suppresses transformation of chicken spleen cells.

I S Chen, H M Temin.   

Abstract

The genome of the highly oncogenic avian retrovirus reticuloendotheliosis virus strain T (REV-T) differs from that of the helper virus reticuloendotheliosis virus strain A by a substitution (rel and a large deletion. Further deletions, constructed in vitro, within the helper-virus-related sequences of REV-T have little effect on the ability of the virus to transform chicken spleen cells in vitro. However, deletions that extend into rel abolish transformation. Substitution of helper-virus-related sequences for the deleted region in the non-rel portion of REV-T also abolishes transformation. Viruses with revertant phenotype were obtained both spontaneously and by construction in vitro from these substituted recombinants. The revertant viruses have various mutations, including deletions and insertions, in the helper-virus-related sequences. Thus the additional helper-virus-related sequences suppress expression of transformation in cis, and the deletion in REV-T seems necessary for expression of the transforming properties of the virus.

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Year:  1982        PMID: 6297744     DOI: 10.1016/0092-8674(82)90410-x

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


  28 in total

1.  Regulation of RNA splicing in gag-deficient mutants of Moloney murine sarcoma virus MuSVts110.

Authors:  M De Mars; D A Sterner; S M Chiocca; N W Biggart; E C Murphy
Journal:  J Virol       Date:  1990-04       Impact factor: 5.103

2.  Multiple regions in the Rous sarcoma virus src gene intron act in cis to affect the accumulation of unspliced RNA.

Authors:  C M Stoltzfus; S J Fogarty
Journal:  J Virol       Date:  1989-04       Impact factor: 5.103

3.  Genetic characterization of human c-rel sequences.

Authors:  E Brownell; S J O'Brien; W G Nash; N Rice
Journal:  Mol Cell Biol       Date:  1985-10       Impact factor: 4.272

4.  Activation of oncogenicity of the c-rel proto-oncogene.

Authors:  B S Sylla; H M Temin
Journal:  Mol Cell Biol       Date:  1986-12       Impact factor: 4.272

5.  Quantitative analysis of gene suppression in integrated retrovirus vectors.

Authors:  M Emerman; H M Temin
Journal:  Mol Cell Biol       Date:  1986-03       Impact factor: 4.272

6.  Acquisition of new proviral copies in avian lymphoid cells transformed by reticuloendotheliosis virus.

Authors:  J Y Zhang; H R Bose
Journal:  J Virol       Date:  1989-03       Impact factor: 5.103

7.  Transforming viruses spontaneously arise from nontransforming reticuloendotheliosis virus strain T-derived viruses as a result of increased accumulation of spliced viral RNA.

Authors:  C K Miller; J E Embretson; H M Temin
Journal:  J Virol       Date:  1988-04       Impact factor: 5.103

8.  Functional interaction between transcriptional elements in the long terminal repeat of reticuloendotheliosis virus: cooperative DNA binding of promoter- and enhancer-specific factors.

Authors:  A Hirano; T Wong
Journal:  Mol Cell Biol       Date:  1988-12       Impact factor: 4.272

9.  Temperature-sensitive transforming mutants of the v-rel oncogene.

Authors:  D W White; T D Gilmore
Journal:  J Virol       Date:  1993-11       Impact factor: 5.103

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

Authors:  I S Chen; K C Wilhelmsen; H M Temin
Journal:  J Virol       Date:  1983-01       Impact factor: 5.103

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