1999
DOI: 10.1073/pnas.96.20.11566
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RETRACTED: Three unrelated viral transforming proteins (vIRF, EBNA2, and E1A) induce the MYC oncogene through the interferon-responsive PRF element by using different transcription coadaptors

Abstract: undersigned authors wish to report the following. ''Despite repeated attempts, we have been unable to repeat the PRF-mediated transcriptional activation of the cMYC promoter by these viral oncoproteins as described in this paper. In contrast, our findings that vIRF (1-3) and EBNA2 (4) interact with p300 and CBP have been shown independently by others. We can no longer support our conclusion of specific viral oncoprotein activation of the cMYC promoter through the PRF element. We regret the confusion that this … Show more

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Cited by 84 publications
(75 citation statements)
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“…As regulators of cell cycle and tumorigenesis, CBP and p300 are targets for viral oncoproteins such as adenovirus E1a, SV40 large T antigen, HTLV-1 Tax, and tumor suppressor p53 (Shikama et al, 1997;Suzuki et al, 1999) which exert their transforming phenotype in part by neutralizing CBP/p300 function. Based on the data presented in this and previous studies I ( Burysek et al, 1999;Jayachandra et al, 1999), HHV-8 encoded vIRF-1 can likewise be considered an oncogene with the capacity to ablate CBP/p300 tumor suppressor activity. In fact, recent studies have demonstrated that vIRF-1 directly interacts with p300, displaces p300/CBP-associated factor from p300 complexes and inhibits p300 histone acetyltransferase activity (Li et al, 2000).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…As regulators of cell cycle and tumorigenesis, CBP and p300 are targets for viral oncoproteins such as adenovirus E1a, SV40 large T antigen, HTLV-1 Tax, and tumor suppressor p53 (Shikama et al, 1997;Suzuki et al, 1999) which exert their transforming phenotype in part by neutralizing CBP/p300 function. Based on the data presented in this and previous studies I ( Burysek et al, 1999;Jayachandra et al, 1999), HHV-8 encoded vIRF-1 can likewise be considered an oncogene with the capacity to ablate CBP/p300 tumor suppressor activity. In fact, recent studies have demonstrated that vIRF-1 directly interacts with p300, displaces p300/CBP-associated factor from p300 complexes and inhibits p300 histone acetyltransferase activity (Li et al, 2000).…”
Section: Discussionmentioning
confidence: 99%
“…It has been demonstrated that vIRF-1, as well as EBNA1 and E1A, not only prevented interferonmediated activation of interferon-stimulated genes but also activated MYC protooncogene (Jayachandra et al, 1999). vIRF-1, in association with an unidenti®ed cellular factor, activates MYC transcription through an ISRE sequence called the plasmacytoma repressor factor (PRF) element located in the upstream of MYC promoter.…”
Section: Discussionmentioning
confidence: 99%
“…This modi®cation alters Tat function in stimulating transcription from viral long terminal repeats (Benkirane et al, 1998;Kiernan et al, 1999;Marzio et al, 1998). Other viral factors such as SV40 T-antigen, papilloma E6, HTLV Tax and KSHV vIRF have been shown to interact with cellular HAT activities (Bex et al, 1998;Eckner et al, 1996;Jayachandra et al, 1999;Patel et al, 1999;Zimmermann et al, 1999). In some cases a clear requirement for HAT activity has been demonstrated, but the coactivator functions of p300 or CBP or as yet uncharacterized functions of P/CAF could also be required by these viral activators.…”
Section: Discussionmentioning
confidence: 99%
“…7 The vIRF protein directly interacts with these DNA -binding proteins to interfere with their functions. For example, vIRF down -regulates MYC proto -oncogene and cyclin-dependent protein kinase inhibitor p21 WAF1 / CIP1 , 2,6 both of which are interferon -responsive genes involved in cell cycle checkpoint and progression. 8 ± 11 Furthermore, we have detected vIRF protein expression in PEL cell lines and KS lesions using a vIRF -specific monoclonal antibody ( unpublished data ).…”
mentioning
confidence: 99%