ArticleRetrovirology2009
Involvement of TORC2, a CREB co-activator, in the in vivo-specific transcriptional control of HTLV-1.
Article in Retrovirology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Exploitation of CREB signaling by HTLV-1 and BLV: A central axis in viral persistence and leukemogenesis.Medical oncology (Northwood, London, England) · 2026Review
- The role of CREB and MAPK signaling pathways in ATLL patients.AIDS research and therapy · 2024Article
- The CREB Regulated Transcription Coactivator 2 Suppresses HIV-1 Transcription by Preventing RNA Pol II from Binding to HIV-1 LTR.Virologica Sinica · 2021Article
- Impact of host immunity on HTLV-1 pathogenesis: potential of Tax-targeted immunotherapy against ATL.Retrovirology · 2019Review
- Hijacking of the O-GlcNAcZYME complex by the HTLV-1 Tax oncoprotein facilitates viral transcription.PLoS pathogens · 2017Article
- SIRT1 Suppresses Human T-Cell Leukemia Virus Type 1 Transcription.Journal of virology · 2015Article
- Group I p21-activated kinases facilitate Tax-mediated transcriptional activation of the human T-cell leukemia virus type 1 long terminal repeats.Retrovirology · 2013Article
- Stabilization of human interferon-α1 mRNA by its antisense RNA.Cellular and molecular life sciences : CMLS · 2013Article
- HTLV tax: a fascinating multifunctional co-regulator of viral and cellular pathways.Frontiers in microbiology · 2012Article
- Cotranscriptional Chromatin Remodeling by Small RNA Species: An HTLV-1 Perspective.Leukemia research and treatment · 2012Article
- The roles of acquired and innate immunity in human T-cell leukemia virus type 1-mediated diseases.Frontiers in microbiology · 2012Article
- Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman T-cell leukemia virus type 1 (HTLV-1) causes adult T -cell leukemia (ATL) but the expression of HTLV-1 is strongly suppressed in the peripheral blood of infected people. However, such suppression, which may explain the long latency in the development of ATL, is readily reversible, and viral expression resumes quickly with ex vivo culture of infected T -cells. To investigate the mechanism of in vivo -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).
resultsGax gene transcription was silenced in vivo but quickly up-regulated in ex vivo culture. Analysis of integrated Gax 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 in vivo, and this returned to normal levels in ex vivo 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.
conclusionThese results suggest that the TORC2 may play an important role in the in vivo -specific transcriptional control of HTLV-1. This study provides a new model for the reversible mechanism that suppresses HTLV-1 expression in vivo 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.
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