HIV molecular immunology database
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|MAb ID||1D9D5 (1D9)|
|Tat Epitope Map|
|Keywords||antibody interactions, binding affinity|
Showing 5 of 5 notes.
Showing 4 of 4 references.
Kanduc2008 Darja Kanduc, Rosario Serpico, Alberta Lucchese, and Yehuda Shoenfeld. Correlating Low-Similarity Peptide Sequences and HIV B-Cell Epitopes. Autoimmun. Rev., 7(4):291-296, Feb 2008. PubMed ID: 18295732. Show all entries for this paper.
Mhashilkar1995 A. M. Mhashilkar, J. Bagley, S. Y. Chen, A. M. Szilvay, D. G. Helland, and W. A. Marasco. Inhibition of HIV-1 Tat-Mediated LTR Transactivation and HIV-1 Infection by Anti-Tat Single Chain Intrabodies. EMBO J., 14:1542-1551, 1995. Anti-Tat intrabodies specific for the N-terminal activation domain of Tat, block Tat-mediated transactivation of the HIV-1 LTR and intracellular trafficking of Tat in mammalian cells. Thus single chain intrabodies can effectively target molecules in the cytoplasm and nuclear compartments of eukaryotic cells and anti-Tat intrabodies may be useful for gene therapy of HIV-1 infection and AIDS. PubMed ID: 7537216. Show all entries for this paper.
Theisen2006 Dietmar M. Theisen, Carola Pongratz, Katja Wiegmann, Francisco Rivero, Oleg Krut, and Martin Krönke. Targeting of HIV-1 Tat Traffic and Function by Transduction-Competent Single Chain Antibodies. Vaccine, 24(16):3127-3136, 12 Apr 2006. PubMed ID: 16497417. Show all entries for this paper.
Valvatne1996 H. Valvatne, A. M. Szilvay, and D. E. Helland. A Monoclonal Antibody Defines a Novel HIV Type 1 Tat Domain Involved in Trans-Cellular Trans-Activation. AIDS Res. Hum. Retroviruses, 12:611-619, 1996. CAT and beta-galactosidase assays, and immunofluorescence analysis were used to study the cellular uptake of the HIV-1 Tat protein. A MAb binding to the basic domain and the RGD sequence inhibits trans- activation by exogenous Tat. The inhibition of the cellular uptake of Tat by an anti-Tat monoclonal antibody and by the serum components implies specific binding of Tat to the cell membrane. PubMed ID: 8743086. Show all entries for this paper.