{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T11:55:12Z","timestamp":1791114912866,"version":"4.1.0"},"reference-count":51,"publisher":"American Society for Microbiology","issue":"24","license":[{"start":{"date-parts":[[2007,12,15]],"date-time":"2007-12-15T00:00:00Z","timestamp":1197676800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2007,12,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Rift Valley fever virus (RVFV) is a member of the genus\n            <jats:italic>Phlebovirus<\/jats:italic>\n            within the family\n            <jats:italic>Bunyaviridae<\/jats:italic>\n            . It can cause severe epidemics among ruminants and fever, myalgia, a hemorrhagic syndrome, and\/or encephalitis in humans. The RVFV M segment encodes the NSm and 78-kDa proteins and two major envelope proteins, Gn and Gc. The biological functions of the NSm and 78-kDa proteins are unknown; both proteins are dispensable for viral replication in cell cultures. To determine the biological functions of the NSm and 78-kDa proteins, we generated the mutant virus arMP-12-del21\/384, carrying a large deletion in the pre-Gn region of the M segment. Neither NSm nor the 78-kDa protein was synthesized in arMP-12-del21\/384-infected cells. Although arMP-12-del21\/384 and its parental virus, arMP-12, showed similar growth kinetics and viral RNA and protein accumulation in infected cells, arMP-12-del21\/384-infected cells induced extensive cell death and produced larger plaques than did arMP-12-infected cells. arMP-12-del21\/384 replication triggered apoptosis, including the cleavage of caspase-3, the cleavage of its downstream substrate, poly(ADP-ribose) polymerase, and activation of the initiator caspases, caspase-8 and -9, earlier in infection than arMP-12. NSm expression in arMP-12-del21\/384-infected cells suppressed the severity of caspase-3 activation. Further, NSm protein expression inhibited the staurosporine-induced activation of caspase-8 and -9, demonstrating that other viral proteins were dispensable for NSm's function in inhibiting apoptosis. RVFV NSm protein is the first identified\n            <jats:italic>Phlebovirus<\/jats:italic>\n            protein that has an antiapoptotic function.\n          <\/jats:p>","DOI":"10.1128\/jvi.01238-07","type":"journal-article","created":{"date-parts":[[2007,10,4]],"date-time":"2007-10-04T00:34:22Z","timestamp":1191458062000},"page":"13335-13345","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":181,"title":["NSm Protein of Rift Valley Fever Virus Suppresses Virus-Induced Apoptosis"],"prefix":"10.1128","volume":"81","author":[{"given":"Sungyong","family":"Won","sequence":"first","affiliation":[{"name":"Departments of Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tetsuro","family":"Ikegami","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. J.","family":"Peters","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology"},{"name":"Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas 77555-1019"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinji","family":"Makino","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Immunology"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)89560-6"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/17.23.6888"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0924-8579(02)00295-9"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.76.12.5937-5948.2002"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.18.9798-9806.2004"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virol.2007.01.046"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.02095-06"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.01420-06"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.16.10420-10428.2005"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.tim.2005.11.003"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4402034"},{"key":"e_1_3_2_13_2","first-page":"73","volume":"56","year":"2007","unstructured":"CDC. 2007. 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