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To investigate the mechanism of <jats:italic>in vivo -<\/jats:italic>specific transcriptional suppression, we established a mouse model in which mice were intraperitoneally administered syngeneic EL4 T -lymphoma cells transduced with a recombinant retrovirus expressing a GFP-Tax fusion protein, Gax, under the control of the HTLV-1 enhancer (EL4-Gax).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>\n              <jats:italic>Gax<\/jats:italic> gene transcription was silenced <jats:italic>in vivo<\/jats:italic> but quickly up-regulated in <jats:italic>ex vivo<\/jats:italic> culture. Analysis of integrated <jats:italic>Gax<\/jats:italic> reporter gene demonstrated that neither CpG methylation of the promoter DNA nor histone modification was associated with the reversible suppression. ChIP-analysis of LTR under suppression revealed reduced promoter binding of TFIIB and Pol-II, but no change in the binding of CREB or CBP\/p300 to the viral enhancer sequence. However, the expression of TORC2, a co-activator of CREB, decreased substantially in the EL4-Gax cells <jats:italic>in vivo<\/jats:italic>, and this returned to normal levels in <jats:italic>ex vivo<\/jats:italic> culture. The reduced expression of TORC2 was associated with translocation from the nucleus to the cytoplasm. A knock-down experiment with siRNA confirmed that TORC2 was the major functional protein of the three TORC-family proteins (TORC1, 2, 3) in EL4-Gax cells.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>These results suggest that the TORC2 may play an important role in the <jats:italic>in vivo<\/jats:italic> -specific transcriptional control of HTLV-1. This study provides a new model for the reversible mechanism that suppresses HTLV-1 expression <jats:italic>in vivo<\/jats:italic> without the DNA methylation or hypoacetylated histones that is observed in the primary cells of most HTLV-1 -infected carriers and a substantial number of ATL cases.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1742-4690-6-73","type":"journal-article","created":{"date-parts":[[2009,8,12]],"date-time":"2009-08-12T14:21:10Z","timestamp":1250086870000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Involvement of TORC2, a CREB co-activator, in the in vivo-specific transcriptional control of HTLV-1"],"prefix":"10.1186","volume":"6","author":[{"given":"Shiwen","family":"Jiang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takefumi","family":"Inada","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masakazu","family":"Tanaka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rika A","family":"Furuta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koh","family":"Shingu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun-ichi","family":"Fujisawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2009,8,11]]},"reference":[{"issue":"6","key":"1078_CR1","doi-asserted-by":"publisher","first-page":"2031","DOI":"10.1073\/pnas.79.6.2031","volume":"79","author":"M Yoshida","year":"1982","unstructured":"Yoshida M, Miyoshi I, Hinuma Y: Isolation and characterization of retrovirus from cell lines of human adult T-cell leukemia and its implication in the disease. 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