       Document 0553
 DOCN  M9620553
 TI    Stimulation of alpha 1 (I) procollagen gene expression in NIH-3T3 cells
       by the human T cell leukemia virus type 1 (HTLV-1) Tax gene.
 DT    9602
 AU    Munoz E; Suri D; Amini S; Khalili K; Jimenez SA; Department of Medicine,
       Jefferson Medical College, Thomas; Jefferson University, Philadelphia,
       Pennsylvania 19107, USA.
 SO    J Clin Invest. 1995 Nov;96(5):2413-20. Unique Identifier : AIDSLINE
       MED/96066708
 AB    The mechanisms that regulate the expression of genes encoding
       extracellular matrix proteins in fibroblasts and other mesenchymal cells
       have remained elusive. Studies from several laboratories have indicated
       that Tax, a trans-regulatory protein from the human T cell leukemia
       virus type I not only augments viral gene expression but also triggers
       the expression of various cellular genes. Here, we examined the
       hypothesis that the expression of collagen genes may also be modulated
       by Tax. NIH-3T3 cells were simultaneously transfected with a Tax
       expressor plasmid and a chimeric construct containing regulatory
       sequences (-804 to +42 bp) of the alpha 1(I) procollagen gene (COL1A1)
       promoter. The results indicated that the promoter activity of the -804
       to bp COL1A1 fragment increased up to 12-fold in cells expressing Tax.
       Deletion analysis revealed that the region of COL1A1 encompassing
       nucleotides -174 to -84 contained the Tax-responsive elements. A gene
       segment encompassing nucleotides -187 to -67, which contained this
       region, proved sufficient to confer Tax inducibility (2.5-fold) to a
       herpes simplex virus thymidine kinase promoter. Stably transfected
       NIH-3T3 cell clones that constitutively produce Tax displayed elevated
       levels of alpha 1(I) procollagen and fibronectin transcripts and
       increased production and accelerated processing of type I procollagen.
       These findings suggest that retroviral proteins may be involved in the
       pathogenesis of idiopathic diseases accompanied by collagen
       overproduction.
 DE    Animal  Gene Expression Regulation  Gene Products, tax/*GENETICS  Gene
       Transfer  Human  HTLV-I/*GENETICS  Mice  Plasmids/GENETICS
       Procollagen/*BIOSYNTHESIS/GENETICS  RNA, Messenger/ANALYSIS  Support,
       Non-U.S. Gov't  Support, U.S. Gov't, P.H.S.  3T3 Cells  JOURNAL ARTICLE

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

