{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T12:07:07Z","timestamp":1791115627931,"version":"4.1.0"},"reference-count":77,"publisher":"American Society of Hematology","issue":"10","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Human immunodeficiency virus type 1 (HIV-1) uses the chemokine receptors CCR5 and CXCR4 as coreceptors for entry. It was recently demonstrated that HIV-1 glycoprotein 120 (gp120) elevated calcium and activated several ionic signaling responses in primary human macrophages, which are important targets for HIV-1 in vivo. This study shows that chemokine receptor engagement by both CCR5-dependent (R5) and CXCR4-dependent (X4) gp120 led to rapid phosphorylation of the focal adhesion-related tyrosine kinase Pyk2 in macrophages. Pyk2 phosphorylation was also induced by macrophage inflammatory protein-1\u03b2 (MIP-1\u03b2) and stromal cell\u2013derived factor-1\u03b1, chemokine ligands for CCR5 and CXCR4. Activation was blocked by EGTA and by a potent blocker of calcium release\u2013activated Ca++(CRAC) channels, but was insensitive to pertussis toxin (PTX), implicating CRAC-mediated extracellular Ca++ influx but not G\u03b1i protein-dependent mechanisms. Coreceptor engagement by gp120 and chemokines also activated 2 members of the mitogen-activated protein kinase (MAPK) superfamily, c-Jun amino-terminal kinase\/stress-activated protein kinase and p38 MAPK. Furthermore, gp120-stimulated macrophages secreted the chemokines monocyte chemotactic protein-1 and MIP-1\u03b2 in a manner that was dependent on MAPK activation. Thus, the gp120 signaling cascade in macrophages includes coreceptor binding, PTX-insensitive signal transduction, ionic signaling including Ca++ influx, and activation of Pyk2 and MAPK pathways, and leads to secretion of inflammatory mediators. HIV-1 Env signaling through these pathways may contribute to dysregulation of uninfected macrophage functions, new target cell recruitment, or modulation of macrophage infection.<\/jats:p>","DOI":"10.1182\/blood.v98.10.2909","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T12:46:47Z","timestamp":1027774007000},"page":"2909-2916","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":119,"title":["HIV-1 gp120 and chemokine activation of Pyk2 and mitogen-activated protein kinases in primary macrophages mediated by calcium-dependent, pertussis toxin\u2013insensitive chemokine receptor signaling"],"prefix":"10.1182","volume":"98","author":[{"given":"Manuela","family":"Del Corno","sequence":"first","affiliation":[{"name":"From the Department of Medicine, University of Pennsylvania School of Medicine, and Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA; Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium; and Laboratory of Virology, Istituto Superiore di Sanita', Rome, Italy."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing-Hua","family":"Liu","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, University of Pennsylvania School of Medicine, and Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA; Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium; and Laboratory of Virology, Istituto Superiore di Sanita', Rome, Italy."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dominique","family":"Schols","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, University of Pennsylvania School of Medicine, and Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA; Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium; and Laboratory of Virology, Istituto Superiore di Sanita', Rome, Italy."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik","family":"de Clercq","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, University of Pennsylvania School of Medicine, and Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA; Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium; and Laboratory of Virology, Istituto Superiore di Sanita', Rome, Italy."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra","family":"Gessani","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, University of Pennsylvania School of Medicine, and Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA; Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium; and Laboratory of Virology, Istituto Superiore di Sanita', Rome, Italy."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce D.","family":"Freedman","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, University of Pennsylvania School of Medicine, and Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA; Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium; and Laboratory of Virology, Istituto Superiore di Sanita', Rome, Italy."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronald G.","family":"Collman","sequence":"additional","affiliation":[{"name":"From the Department of Medicine, University of Pennsylvania School of Medicine, and Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA; Rega Institute for Medical Research, Katholieke 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