{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:18:06Z","timestamp":1791397086049,"version":"4.3.3"},"reference-count":50,"publisher":"Rockefeller University Press","issue":"2","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2003,10,27]]},"abstract":"<jats:p>The cellular pathways required for herpes simplex virus (HSV) invasion have not been defined. To test the hypothesis that HSV entry triggers activation of Ca2+-signaling pathways, the effects on intracellular calcium concentration ([Ca2+]i) after exposure of cells to HSV were examined. Exposure to virus results in a rapid and transient increase in [Ca2+]i. Pretreatment of cells with pharmacological agents that block release of inositol 1,4,5-triphosphate (IP3)\u2013sensitive endoplasmic reticulum stores abrogates the response. Moreover, treatment of cells with these pharmacological agents inhibits HSV infection and prevents focal adhesion kinase (FAK) phosphorylation, which occurs within 5 min after viral infection. Viruses deleted in glycoprotein L or glycoprotein D, which bind but do not penetrate, fail to induce a [Ca2+]i response or trigger FAK phosphorylation. Together, these results support a model for HSV infection that requires activation of IP3-responsive Ca2+-signaling pathways and that is associated with FAK phosphorylation. Defining the pathway of viral invasion may lead to new targets for anti-viral therapy.<\/jats:p>","DOI":"10.1083\/jcb.200301084","type":"journal-article","created":{"date-parts":[[2003,10,20]],"date-time":"2003-10-20T20:41:32Z","timestamp":1066682492000},"page":"283-293","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":124,"title":["Herpes simplex virus triggers activation of calcium-signaling pathways"],"prefix":"10.1083","volume":"163","author":[{"given":"Natalia","family":"Cheshenko","sequence":"first","affiliation":[{"name":"Department of Pediatrics and Microbiology, Mount Sinai School of Medicine, New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"Del Rosario","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Microbiology, Mount Sinai School of Medicine, New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Craig","family":"Woda","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Microbiology, Mount Sinai School of Medicine, New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Marcellino","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Microbiology, Mount Sinai School of Medicine, New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa M.","family":"Satlin","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Microbiology, Mount Sinai School of Medicine, New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Betsy C.","family":"Herold","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Microbiology, Mount Sinai School of Medicine, New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2003,10,20]]},"reference":[{"key":"2023072905204363400_BIB1","doi-asserted-by":"crossref","first-page":"597","DOI":"10.1084\/jem.190.5.597","volume":"190","year":"1999","journal-title":"J. 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