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Titolo:
SMALL-MOLECULE INHIBITOR OF HIV-1 CELL-FUSION BLOCKS CHEMOKINE RECEPTOR-MEDIATED FUNCTION
Autore:
HOWARD OMZ; KORTE T; TARASOVA NI; GRIMM M; TURPIN JA; RICE WG; MICHEJDA CJ; BLUMENTHAL R; OPPENHEIM JJ;
Indirizzi:
POB B FREDERICK MD 21702 SAIC FREDERICK,INTRAMURAL RES SUPPORT PROGRAM FREDERICK MD 00000 NCI,FREDERICK CANC RES & DEV CTR,LAB ANTIVIRAL DRUG MECHANISMS,SAIC FREDERICK FREDERICK MD 21701 NCI,FREDERICK CANC RES & DEV CTR,MOL IMMUNOREGULAT LAB,DIV BASIC SCI FREDERICK MD 21701 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MOL ASPECTS DRUG DESIGN SECT FREDERICK MD 21701 NCI,FREDERICK CANC RES & DEV CTR,LAB EXPT & COMPUTAT BIOL,DIV BASIC SCI FREDERICK MD 21701
Titolo Testata:
Journal of leukocyte biology
fascicolo: 1, volume: 64, anno: 1998,
pagine: 6 - 13
SICI:
0741-5400(1998)64:1<6:SIOHCB>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN RANTES; BINDING; INTERLEUKIN-8; INTERVENTION; DISSOCIATION; ANTAGONIST; ENTRY;
Keywords:
CHEMOKINE INHIBITOR; ANTI-HIV-1; CHEMOKINE RECEPTOR INTERNALIZATION;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
O.M.Z. Howard et al., "SMALL-MOLECULE INHIBITOR OF HIV-1 CELL-FUSION BLOCKS CHEMOKINE RECEPTOR-MEDIATED FUNCTION", Journal of leukocyte biology, 64(1), 1998, pp. 6-13

Abstract

The intersection of the HIV and the chemokine fields began with the observation that HIV entry into cells could be blocked by certain chemokines. Subsequent work showed that HIV entry is dependent on the presence of specific chemokine receptors, These observations led us to evaluate a series of compounds, ureido analogs of distamycin previously reported to block HIV entry into cells in vitro, for chemokine antagonist activity, One of the distamycin analogs, [N,4'-di[pyrrole-2-carboxamide-1,1'-dimethyl]]-6,8 napthalenedisulfonic acid] hexasodium salt (NSC 651016), is shown here to inhibit syncytia formation and cell fusion, Mechanistic studies showed that this inhibition was not due to conformational changes in gp120-gp41 induced by target cell CDP and chemokine co-receptor and was therefore not due to interference with binding of HIV-1. Additional mechanistic studies demonstrated that NSC 651016 inhibited chemokine binding to specific chemokine receptors, induced CXCR4 and CCR5 receptor internalization, and inhibited chemokine-induced chemotaxis by macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta, RANTES, and stromal-derived factor-1 alpha but not monocyte chemotactic protein-1, Thus, we describe a novel compound that inhibits in vivo replication of HIV-1 by down-regulation of coreceptors, These data lead us to propose that NSC 651016 may have in vivo anti-inflammatory activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 18:05:20