{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T01:34:15Z","timestamp":1788572055230,"version":"build-2803163510"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,6,29]],"date-time":"2007-06-29T00:00:00Z","timestamp":1183075200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2007,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>While a number of studies have documented the neurotropism of Japanese encephalitis virus (JEV), little is known regarding the molecular mechanism of neuronal death following viral infection. The tumor necrosis factor receptor (TNFR)\u2010associated death domain (TRADD) has been suggested to be the crucial signal adaptor that mediates all intracellular responses from TNFR\u20101. Using mouse (Neuro2a) and human (SK\u2010N\u2010SH) neuroblastoma cell lines, we have shown that the altered expression of TNFR\u20101 and TRADD following JEV infection regulates the downstream apoptotic cascades. Activation of TRADD led to mitochondria\u2010mediated neuronal apoptosis. As TRADD\u2010knockout animals or deficient cell lines are unavailable, it has been difficult to definitively address the physiological role of TRADD in diseases pathology following JEV infection. We circumvented this problem by silencing TRADD expression with small\u2010interfering RNA (<jats:italic>si<\/jats:italic>RNA) and have found that TRADD is required for TNFR\u20101\u2010initiated neuronal apoptosis following <jats:italic>in vitro<\/jats:italic> infection with JEV. Interestingly, <jats:italic>si<\/jats:italic>RNA against TRADD also decreased the viral load in Neuro2a cells. Furthermore, <jats:italic>si<\/jats:italic>RNA against TRADD increased the survival of JEV\u2010infected mice by altering the expression of pro apoptotic versus antiapoptotic molecules. These studies show that the engagement of TNFR\u20101 and TRADD following JEV infection plays a crucial role in neuronal apoptosis.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2007.04790.x","type":"journal-article","created":{"date-parts":[[2007,7,31]],"date-time":"2007-07-31T09:06:22Z","timestamp":1185872782000},"page":"771-783","source":"Crossref","is-referenced-by-count":62,"title":["Tumor necrosis factor receptor\u20101\u2010induced neuronal death by TRADD contributes to the pathogenesis of Japanese encephalitis"],"prefix":"10.1111","volume":"103","author":[{"given":"Vivek","family":"Swarup","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sulagna","family":"Das","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soumya","family":"Ghosh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anirban","family":"Basu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2007,6,29]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.micinf.2005.05.023"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.281.5381.1305"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/nn1166"},{"key":"e_1_2_7_5_1","doi-asserted-by":"crossref","first-page":"6071","DOI":"10.1523\/JNEUROSCI.22-14-06071.2002","article-title":"The type 1 interleukin\u20101 receptor is essential for the efficient activation of microglia and the induction of multiple proinflammatory mediators in response to brain injury","volume":"22","author":"Basu A.","year":"2002","journal-title":"J. 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