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IFN-gamma gene expression is controlled by the architectural transcription factor HMGA1

  1. Author:
    Chau, K. Y.
    Keane-Myers, A. M.
    Fedele, M.
    Ikeda, Y.
    Creusot, R. J.
    Menozzi, L.
    Cousins, D. J.
    Manfioletti, G.
    Feigenbaum, L.
    Fusco, A.
    Ono, S. J.
  2. Author Address

    Univ Coll London, Inst Ophthalmol, Dept Immunol, London EC1V 9EL, England. Moorfields Eye Hosp, NHS Fdn Trust, London EC1V 9EL, England. NIAID, Lab Allerg Dis, Eosinophil Biol Sect, NIH, Rockville, MD USA. Univ Naples Federico II, CNR, Ist Endocrinol & Oncol Sperimentale, Dipartimento Biol & Patol Cellulare & Mol, Naples, Italy. Univ Coll London, Windeyer Inst Med Sci, Dept Immunol & Mol Pathol, London WC1E 6BT, England. Univ London Kings Coll, GKT Sch Med, Dept Asthma Allergy & Resp Sci, London WC2R 2LS, England. Univ Trieste, Dipartimento Biochim Biofis & Chim Macromol, I-34127 Trieste, Italy. NCI, Sci Applicat Int Corp, Frederick, MD 21701 USA Ono, SJ, Univ Coll London, Inst Ophthalmol, Dept Immunol, 11-43 Bath St, London EC1V 9EL, England
    1. Year: 2005
    2. Date: MAR
  1. Journal: International Immunology
    1. 17
    2. 3
    3. Pages: 297-306
  2. Type of Article: Article
  1. Abstract:

    We report for the first time that IFNG gene expression requires high mobility group (HMG)A1, the architectural transcription factor mediating enhanceosome formation. This finding is supported by our direct studies of T cells isolated from the HMGA1-transgenic mice displaying an up-regulation of IFN-gamma production and of HMGA1-deficient mice exhibited a decreased IFN-gamma induction. In parallel transfection studies in EL4 cells, we observed elevated IFNG gene promoter activity in cells stably over-expressing HMGA1 and a reduction of such activity in cells expressing dominant-negative HMGA1. In vitro binding assays further demonstrated a specific interaction of HMGA1 to defined regions of the IFNG gene proximal promoter

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