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The long terminal repeat of the intracisternal A particle as a target for transactivation by oncogene products


, : The long terminal repeat of the intracisternal A particle as a target for transactivation by oncogene products. Journal of Virology 57(3): 998-1003

It has been shown recently that the c-mos oncogene becomes activated in myeloma XRPC-24 via insertion of an intracisternal A particle (IAP) long terminal repeat (LTR). The inserted LTR serves as a promoter from which transcription of the 3' rearranged c-mos initiates. The insertion is in a head-to-head orientation such that the transcriptional orientations of the IAP and the 3' rearranged c-mos are opposite. It has already been shown that this IAP LTR has two promoters, one transcribing the IAP genome and the other transcribing the rearranged c-mos. Since the IAP genomes are actively transcribed in mouse myelomas but not in normal cells, it was interesting to test whether transcriptional activation of the IAP occurs in the presence of active oncogene products, especially nuclear ones. The 5' LTR of the IAP inserted in myeloma XRPC-24 was chosen as a convenient model to test the effect of viral and cellular oncogene products. These included simian virus 40 (SV40) large-T antigen, the adenovirus early 1A (E1A) gene product, the myc gene product, and p53. The LTR was coupled to the bacterial gene coding for chloramphenicol acetyltransferase (CAT) in two orientations, and the levels of CAT directed by the LTR promoters were assayed in either the presence or the absence of the oncogene products. The levels of CAT directed by the 5' LTR promoter transcribing the IAP were significantly elevated in the presence of SV40 large-T antigen, the adenovirus E1A and myc gene products, and p53. The promoter transcribing the rearranged c-mos was transactivated by SV40 large-T antigen and the adenovirus E1A gene product. The results indicate that oncogene products may have an important role in turning on promoters of other genes. The IAP LTR may serve as a useful model for studying the effect of various gene products on promoters which are known to be activated in the malignant state.

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Accession: 006712067

PMID: 2936901

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Related references

Galien, R.; Mercier, G.; Garcette, M.; Emanoil-Ravier, R., 1991: ras oncogene activates the intracisternal A particle long terminal repeat promoter through a c-AMP response element. To understand the mechanism responsible for the high expression of Intracisternal A Particles (IAP) in murine cells transformed by the Kirsten Mouse Sarcoma Virus (Ki-MSV), we have investigated the effect of p21ras on IAP transcription. By transie...

Horowitz M.; Luria S.; Rechavi G.; Givol D., 1984: Mechanism of activation of the mouse c mos oncogene by the long terminal repeat of an intracisternal a particle gene. In the mouse myeloma XRPC-24 the DNA of an intracisternal A-particle (IAP) is inserted within the coding region of c-mos. This insertion splits the c-mos into a 3' rc-mos and a 5' rc-mos separated by .apprx. 4.7 kb [kilobase pair] of IAP...

Galien R.; Mercier G.; Garcette M.; Emanoil Ravier R., 1991: Ras oncogene activates the intracisternal a particle long terminal repeat promoter through a cyclic amp response element. To understand the mechanism responsible for the high expession of Intracisternal A Particles (IAP) in murine cells transformed by the Kirsten Mouse Sarcoma Virus (Ki-MSV), we have investigated the effect of p21ras on IAP transcription. By transien...

Mowat, M.; Sauder, M.; Pereira, D., 1990: The activated form of p53 is not a transactivator of the intracisternal A particle long terminal repeat promoter. Published observations have suggested that the activated form of p53 protein could transactivate the Intracisternal A particle long terminal repeat promoter (IAP-LTR). In this paper we demonstrate that the increased expression from this promoter w...

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