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Oncogene 1997 May 1;14(17):2071-2078

Characterization of peripheral blood T-lymphocytes transduced with HTLV-I Tax mutants with different trans-activating phenotypes.

Akagi T, Ono H, Nyunoya H, Shimotohno K

Virology Division, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.

Tax1, a transcriptional trans-activator of the Human T-cell leukemia virus type I (HTLV-I), induces the expression of many cellular genes through interaction with at least three distinct cellular transcription factors; CREB/ATF, NF-kappaB, and SRF. This Tax1-induced activation of cellular genes is considered to be a critical event in T-cell transformation by HTLV-I. To elucidate the role of each Tax1-inducible transcriptional pathway in T-cell transformation, we introduced Tax1 mutants with different trans-activating phenotypes into peripheral blood lymphocytes (PBL) by retroviral vectors. Analysis of these PBLs revealed that activation of the NF-kappaB pathway is sufficient to promote the growth response to IL-2. However, for the clonal expansion of CD4+ T-cells, which is a characteristic result of HTLV-I infection, activation of the CREB/ATF and SRF pathways is also required.

MeSH Terms:

• Cell Division/drug effects
• Clone Cells
• CD4-Positive T-Lymphocytes/virology
• CD4-Positive T-Lymphocytes/metabolism
• CD4-Positive T-Lymphocytes/drug effects
• DNA-Binding Protein, Cyclic AMP-Responsive/physiology*
• DNA-Binding Proteins/physiology*
• Gene Expression Regulation, Viral*
• Gene Products, tax/physiology*
• Gene Products, tax/genetics
• Genes, pX*
• Human
• HTLV-I/genetics*
• Interleukin-2/pharmacology
• Lymphocyte Transformation/drug effects
• Nuclear Proteins/physiology*
• NF-kappa B/physiology*
• Phenotype
• Point Mutation
• Support, Non-U.S. Gov't
• T-Lymphocytes/virology*
• T-Lymphocytes/metabolism
• T-Lymphocytes/drug effects
• Trans-Activation (Genetics)*

Substances:

• NF-kappa B
• Nuclear Proteins
• Interleukin-2
• Gene Products, tax
• DNA-Binding Proteins
• DNA-Binding Protein, Cyclic AMP-Responsive
• serum response factor

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