Document 0571
 DOCN  M9590571
 TI    Peptide T from human immunodeficiency virus does not interact with VIP
       receptor-effector system in immunocompetent cells of rat and mouse.
 DT    9509
 AU    Pozo D; Segura JJ; Guerrero JM; Calvo JR; Department of Medical
       Biochemistry and Molecular Biology,; University of Seville School of
       Medicine, Spain.
 SO    Biosci Rep. 1994 Oct;14(5):251-7. Unique Identifier : AIDSLINE
       MED/95290624
 AB    Human immunodeficiency virus (HIV) infection is initiated by attachment
       of the virus to specific target cells. An octapeptide sequence contained
       within the envelope of HIV, peptide T, mediates the viral binding. Since
       there is an appreciable structural similarity between peptide T and an
       eight amino acid sequence of VIP, it is interesting to investigate the
       interaction of peptide T with the VIP receptor-effector system of
       immunocompetent cells from both rat and mouse. In this paper, we show
       the lack of interaction between peptide T and VIP receptor-effector
       system in peripheral blood lymphocytes, spleen lymphocytes and
       macrophages of rat and in macrophages of mouse. These results do not
       support the hypothesis that HIV through peptide T may interact with the
       VIP receptor-effector system present in immunocompetent cells.
 DE    Animal  Binding, Competitive  Cells, Cultured  Cyclic AMP/BIOSYNTHESIS
       Human  HIV/*METABOLISM  Lymphocytes/DRUG EFFECTS/*METABOLISM
       Macrophages/DRUG EFFECTS/*METABOLISM  Mice  Peptide
       T/*METABOLISM/PHARMACOLOGY  Rats  Rats, Wistar  Support, Non-U.S. Gov't
       Vasoactive Intestinal Peptide/*METABOLISM  JOURNAL ARTICLE

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       protected by Copyright Law (Title 17, U.S.Code).