Document 0108
 DOCN  M9470108
 TI    Tax proteins of human T-cell leukemia virus type 1 and 2 induce
       expression of the gene encoding erythroid-potentiating activity (tissue
       inhibitor of metalloproteinases-1, TIMP-1).
 DT    9409
 AU    Uchijima M; Sato H; Fujii M; Seiki M; Department of Molecular Virology
       and Oncology, Kanazawa; University, Ishikawa, Japan.
 SO    J Biol Chem. 1994 May 27;269(21):14946-50. Unique Identifier : AIDSLINE
       GENBANK/D26513
 AB    A growth factor-like activity for erythroid cells
       (erythroid-potentiating activity) is produced by the T-cells infected
       with human T-cell leukemia virus type 2 (HTLV-2) (Gasson, J. C., Golde,
       D. W., Kaufman, S. E., Westbrook, C. A., Hewick, R. M., Kaufmann, R. J.,
       Wong, G. G., Temple, P. A., Leary, A. C., Brown, E. L., Orr, E. C., and
       Clark, S. C. (1985) Nature 315, 768-771) and is reportedly identical
       with tissue inhibitors of matrix metalloproteinases-1 (TIMP-1)
       (Docherty, A. J. P., Lyons, A., Smith, B. J., Wright, E. M., Stephens,
       P. E., Harris, T. J. R., Murphy, G., and Reynolds, J. J. (1985) Nature
       318, 66-69). We found that adult T-cell leukemia cell lines infected
       with HTLV-1 also express high levels of a TIMP-1 transcript. A viral
       transactivator of HTLV-1, Tax1, in a human T-cell line (Jurkat), was
       sufficient to stimulate transcription of the TIMP-1 gene. Deletion and
       mutation analysis of the TIMP-1 gene promoter showed that the AP-1
       binding site in the 38-base pair sequence conserved between the human
       and mouse genes was essential for activation by Tax1. The transactivator
       of HTLV-2 also stimulated the promoter through the same cis-element. The
       reported growth-promoting activity of TIMP-1 against erythroid cells and
       potentially against HTLV-1-infected T-cells may modulate the clinical
       course of adult T-cell leukemia.
 DE    Animal  Base Sequence  Binding Sites  Cells, Cultured  *Gene Expression
       Regulation, Viral  Gene Products, tax/*PHYSIOLOGY
       Glycoproteins/*GENETICS  Human  HTLV-I/*METABOLISM  HTLV-II/*METABOLISM
       Lymphocytes/MICROBIOLOGY  Mice  Molecular Sequence Data  Nuclear
       Proteins/METABOLISM  Proto-Oncogene Proteins/METABOLISM  Proto-Oncogene
       Proteins c-jun/METABOLISM  RNA, Messenger/METABOLISM  Support, Non-U.S.
       Gov't  Trans-Activation (Genetics)  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).