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Titolo:
The synthetic peptide WKYMVm attenuates the function of the chemokine receptors CCR5 and CXCR4 through activation of formyl peptide receptor-like 1
Autore:
Li, BQ; Wetzel, MA; Mikovits, JA; Henderson, EE; Rogers, TJ; Gong, WH; Li, YY; Ruscetti, FW; Wang, JM;
Indirizzi:
NCI, LMI, DBS, FCRDC, Frederick, MD 21702 USA NCI Frederick MD USA 21702NCI, LMI, DBS, FCRDC, Frederick, MD 21702 USA SAIC Frederick, Immunogenet Mol Lab, Intramural Res Support Program, Frederick, MD USA SAIC Frederick Frederick MD USA l Res Support Program, Frederick, MD USA SAIC Frederick, Immunogenet Mol Lab, Lab Antiviral Drug Mechanism, NCI Screening Technol Branch, Frederick, MD USA SAIC Frederick Frederick MD USA eening Technol Branch, Frederick, MD USA Temple Univ, Sch Med, Dept Microbiol & Immunol, Philadelphia, PA 19122 USATemple Univ Philadelphia PA USA 19122 Immunol, Philadelphia, PA 19122 USA
Titolo Testata:
BLOOD
fascicolo: 10, volume: 97, anno: 2001,
pagine: 2941 - 2947
SICI:
0006-4971(20010515)97:10<2941:TSPWAT>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
LIPOXIN A(4) RECEPTOR; SERUM AMYLOID-A; HUMAN MONOCYTES; STABLE ANALOGS; DESENSITIZATION; CELLS; 7-TRANSMEMBRANE; IDENTIFICATION; MOBILIZATION; BLOCKS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Wang, JM NCI, LMI, DBS, FCRDC, Bldg 560,Rm 31-40, Frederick, MD 21702 USA NCI Bldg 560,Rm 31-40 Frederick MD USA 21702 derick, MD 21702 USA
Citazione:
B.Q. Li et al., "The synthetic peptide WKYMVm attenuates the function of the chemokine receptors CCR5 and CXCR4 through activation of formyl peptide receptor-like 1", BLOOD, 97(10), 2001, pp. 2941-2947

Abstract

The G protein-coupled 7 transmembrane (STM) chemoattractant receptors can be inactivated by heterologous desensitization. Earlier work showed that formly peptide receptor-like 1 (FPRL1), an STM receptor with low affinity forthe bacterial chemotactic, peptide formyl-methionyl-leucyl-phenylalamine (fMLF), is activated by peptide domains derived from the human immunodeficiency virus (HIV)-1 envelope glycoprotein gp120 and its activation results indesensitization and downregulation of the chemokine receptors CCR5 and CXCR4 from monocyte surfaces. This study Investigated the possibility of interfering with the function of CCR5 or CXCR4 as HIV-1 coreceptors by activating FPRL1. Cell lines were established expressing FPRL1 in combination with CD4/CXCR4 or CD4/CCR5 and the effect of a synthetic peptide, WKYMVm, a potent activator of formyl peptide receptors with preference for FPRL1 was determined. Both CXCR4 and CCR5 were desensitized by activation of the cells with WKYMVm via a staurosporine-sensitive pathway. This desensitization of CXCR4 and CCR5 also attenuated their capacity as the fusion cofactors for HIV-1 envelope glycoprotein and resulted in a significant inhibition of p24 production by cell lines infected with HIV-1 that use CCR5 or CXCR4 as coreceptors. Furthermore, WKYMVm inhibited the infection of human peripheral monocyte-derived macrophages and CD4(+) T lymphocytes by R5 or X4 strains of HIV-1, respectively. These results indicate that heterologous desensitization of CCR5 and CXCR4 by an FPRL1 agonist attenuates their major biologic functions and suggest an approach to the development of additional anti-HIV-1 agents. (Blood. 2001;97:2941-2947) (C) 2001 by The American Society of Hematology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 15:07:03