HTLV-I LTR 21 bp repeat-specific and neuroglial cell-specific DNA-protein complexes (Meeting abstract). NLM AIDSLINE Important note: Information in this article was accurate in 1994. The state of the art may have changed since the publication date.

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HTLV-I LTR 21 bp repeat-specific and neuroglial cell-specific DNA-protein complexes (Meeting abstract).

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
Tillmann M; Hinkel R; Wigdahl B; Dept. of Microbiology and Immunology, Pennsylvania State Univ.; Coll. of Medicine, Hershey, PA

Abstract: 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.
Keywords: Amino Acid Sequence DNA/*ANALYSIS DNA-Binding Proteins/GENETICS Gene Products, tax/GENETICS Human HIV Enhancer HIV Long Terminal Repeat/*GENETICS HTLV-I/*GENETICS Neuroglia/CYTOLOGY/METABOLISM NF-kappa B/GENETICS Trans-Activation (Genetics) ABSTRACT

KWDaminoacidsequencedna/KWDanalysisdna-bindingproteins/geneticsgeneproducts,tax/geneticshumanhivenhancerhivlongterminalrepeat/KWDgeneticshtlv-i/KWDgeneticsneuroglia/cytology/metabolismnf-kappab/geneticstrans-activation(genetics)abstract
940930
M9491059

Copyright © 1994 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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