Regulatory and coding potential of the mouse mammary tumor virus long terminal redundancy.
AUTOR(ES)
Donehower, L A
RESUMO
Molecular clones containing the 3' half of newly integrated mouse mammary tumor virus (MMTV) DNA with adjacent mouse cellular sequences were characterized. In addition, we cloned the long terminal redundancy joint from the unintegrated circular form of MMTV DNA. The entire nucleotide sequence of the integrated and part of the unintegrated terminal redundancy was determined; this allowed us to delineate the boundaries of the MMTV long terminal redundancy, which comprises 1,327 base pairs. The position of possible RNA polymerase II initiation and termination signals corresponded closely to the expected regions of viral RNA initiation and termination specified by current models. The MMTV long terminal redundancy also contained a large open reading frame with sufficient information for a protein of 198 amino acids. Initial comparison of flanking 3' cellular sequences from three independent integrated clones suggested there was no host sequence specificity in the MMTV integration event. However, specificity of integration with respect to viral sequences was precise.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=170999Documentos Relacionados
- Further Evidence for the Protein Coding Potential of the Mouse Mammary Tumor Virus Long Terminal Repeat: Nucleotide Sequence of an Endogenous Proviral Long Terminal Repeat
- Conservation of protein coding potential in the long terminal repeats of exogenous and endogenous mouse mammary tumor viruses.
- Androgen regulation by the long terminal repeat of mouse mammary tumor virus.
- The region of mouse mammary tumor virus DNA containing the long terminal repeat includes a long coding sequence and signals for hormonally regulated transcription.
- Mouse mammary tumor virus proviruses in T-cell lymphomas lack a negative regulatory element in the long terminal repeat.
