{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T16:44:00Z","timestamp":1781109840605,"version":"3.54.1"},"reference-count":31,"publisher":"National Academy of Sciences","issue":"15","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1997,7,22]]},"abstract":"<jats:p>\n                    An earlier report showed that a disabled mutant lacking both copies of the major regulatory gene (\u03b14) of herpes simplex virus 1 induced DNA degradation characteristic of apoptosis in infected cells, whereas the wild-type virus protected cells from apoptosis induced by thermal shock. More extensive analyses of the disabled mutant revealed a second mutation which disabled U\n                    <jats:sub>S<\/jats:sub>\n                    3, a viral gene encoding a protein kinase known to phosphorylate serine\/threonine within a specific arginine-rich consensus sequence. Analyses of cells infected with a viral mutant carrying a wild-type \u03b14 gene but from which the U\n                    <jats:sub>S<\/jats:sub>\n                    3 gene had been deleted showed that it induced fragmentation of cellular DNA, whereas a recombinant virus in which the deleted sequences of the U\n                    <jats:sub>S<\/jats:sub>\n                    3 gene had been restored did not cause the cellular DNA to fragment. These results point to the protein kinase encoded by the U\n                    <jats:sub>S<\/jats:sub>\n                    3 gene as the principal viral product required to block apoptosis.\n                  <\/jats:p>","DOI":"10.1073\/pnas.94.15.7891","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:32:33Z","timestamp":1027679553000},"page":"7891-7896","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":233,"title":["The herpes simplex virus 1 protein kinase U\n                    <sub>S<\/sub>\n                    3 is required for protection from apoptosis induced by the\u2009virus"],"prefix":"10.1073","volume":"94","author":[{"given":"Rosario","family":"Leopardi","sequence":"first","affiliation":[{"name":"The Marjorie B. Kovler Viral Oncology Laboratories, University of Chicago, 910 East 58th Street, Chicago IL 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles","family":"Van Sant","sequence":"additional","affiliation":[{"name":"The Marjorie B. Kovler Viral Oncology Laboratories, University of Chicago, 910 East 58th Street, Chicago IL 60637"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernard","family":"Roizman","sequence":"additional","affiliation":[{"name":"The Marjorie B. 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