PMID: 12758176May 22, 2003Paper

Mutations that abrogate transactivational activity of the feline leukemia virus long terminal repeat do not affect virus replication

Virology
Ana L AbujamraSajal K Ghosh

Abstract

The U3 region of the LTR of oncogenic Moloney murine leukemia virus (Mo-MuLV) and feline leukemia viruses (FeLV) have been previously reported to activate expression of specific cellular genes in trans, such as MHC class I, collagenase IV, and MCP-1, in an integration-independent manner. It has been suggested that transactivation of these specific cellular genes by leukemia virus U3-LTR may contribute to the multistage process of leukemogenesis. The U3-LTR region, necessary for gene transactivational activity, also contains multiple transcription factor-binding sites that are essential for normal virus replication. To dissect the promoter activity and the gene transactivational activity of the U3-LTR, we conducted mutational analysis of the U3-LTR region of FeLV-A molecular clone 61E. We identified minimal nucleotide substitution mutants on the U3 LTR that did not disturb transcription factor-binding sites but abrogated its ability to transactivate the collagenase gene promoter. To determine if these mutations actually have altered any uncharacterized important transcription factor-binding site, we introduced these U3-LTR mutations into the full-length infectious molecular clone 61E. We demonstrate that the mutant virus was rep...Continue Reading

References

Jan 1, 1992·Cancer Investigation·L J RezankaJ C Neil
Sep 1, 1982·Molecular and Cellular Biology·C M GormanB H Howard

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Citations

Jul 26, 2012·Journal of the American Chemical Society·Seth LilavivatKenneth J Woycechowsky
Feb 9, 2008·Emerging Infectious Diseases·Meredith A BrownStephen J O'Brien
Apr 2, 2009·FEBS Letters·Lora W FormanSajal K Ghosh
Jul 1, 2011·Veterinary Immunology and Immunopathology·H StewartB J Willett
Jun 15, 2014·The Veterinary Journal·Julia Beatty

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