Document 1063
 DOCN  M9471063
 TI    HTLV-I LTR 21 bp repeat-specific and neuroglial cell-specific
       DNA-protein complexes (Meeting abstract).
 DT    9409
 AU    Tillmann M; Hinkel R; Wigdahl B; Dept. of Microbiology and Immunology,
       Pennsylvania State Univ.; Coll. of Medicine, Hershey, PA
 SO    International Association for Comparative Research on Leukemia and
       Related Diseases, 16th Symposium. July 11-16, 1993, Montreal, Quebec,
       Canada, A54, 1993.. Unique Identifier : AIDSLINE ICDB/94698652
 AB    Human T-cell leukemia virus type I (HTLV-I) is an etiologic agent of
       adult T-cell leukemia and a chronic neurologic disorder, tropical
       spastic paraparesis. An HTLV-I-encoded protein, Tax, is capable of
       transcriptionally trans-activating HTLV-I by interacting with specific
       sequences in the HTLV-I long terminal repeat (LTR) which comprise an
       inducible enhancer containing three imperfect tandem repeats of a 21 bp
       sequence. Evidence suggests that Tax is incapable of directly
       interacting with DNA; therefore, Tax most likely regulates transcription
       via interaction with cellular factors. Characterization of the cellular
       factors which interact with the 21 bp repeats is essential to
       understanding the molecular mechanisms involved in Tax-mediated
       trans-activation as well as the involvement of Tax and the LTR in the
       cellular tropism of HTLV-I. Utilizing the electrophoretic mobility shift
       assay (EMSA), we detect both 21 bp repeat-specific and neuroglial
       cell-specific DNA-protein complexes. When nuclear extracts derived from
       cells of lymphoid (Jurkat), monocytoid (U937), neuronal (IMR-32), and
       glial (U-373 MG) cell origin are reacted with each of the three 21 bp
       repeats, several 21 bp repeat-specific DNA-protein complexes are
       detected. Results from EMSA competition analyses utilizing unlabeled 21
       bp repeats as competitor DNAs indicate a difference in the ability of
       each unlabeled 21 bp repeat to compete for the specific DNA-protein
       complexes formed between the nuclear extracts and each of the
       radiolabeled 21 bp repeats. In each case, the most effective competitor
       is the homologous, unlabeled 21 bp repeat. Additional results from EMSA
       competition assays utilizing oligonucleotides containing the consensus
       sequence for CRE, Ap-2, NF-kappa B, or Sp1 demonstrate that, of the
       specific DNA-protein complexes, there is differential competition for
       complex formation with each of the three 21 bp repeats. These studies
       indicate that each of the three 21 bp Tax-responsive elements may be
       unique with respect to their participation in specific DNA-protein
       complex formation. In addition to detecting 21 bp repeat-specific
       DNA-protein complexes, neuroglial cell type-specific DNA-protein
       complexes are also detected. A unique DNA-protein complex is detected
       when nuclear extracts derived from IMR-32 and U373-MG cells are reacted
       with the middle 21 bp repeat. Furthermore, one of the specific
       DNA-protein complexes detected when the nuclear extracts derived from
       Jurkat, U937, and IMR-32 cell lines are reacted with each of the three
       21 bp repeats is not detected when nuclear extracts derived from U-373
       MG cells are reacted with each of the three 21 bp repeats.
       Characterization of the 21 bp repeat-specific and neuroglial
       cell-specific DNA-protein complexes is currently under investigation.
 DE    Amino Acid Sequence  DNA/*ANALYSIS  DNA-Binding Proteins/GENETICS  Gene
       Products, tax/GENETICS  HIV Enhancer  HIV Long Terminal Repeat/*GENETICS
       HTLV-I/*GENETICS  Human  NF-kappa B/GENETICS
       Neuroglia/CYTOLOGY/METABOLISM  Trans-Activation (Genetics)  MEETING
       ABSTRACT

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