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IMSUT & RCASTGCOE Program Seminar< Global Education Seminar >

Date and Time:October 9&s_comma; 2009 15:00 - 17:00
Venue : 1st Building&s_comma; 2F seminar room&s_comma; Univ.Tokyo&s_comma; Inst.Med.Sci.
(Subway Namboku/Mita line&s_comma; Shirokane-dai station)
Speaker:Edward S. Mocarski&s_comma; Jr. Ph.D.
Position : Distinguished Fellow&s_comma; Woodruff Professor of Microbiology
and Immunology
Affiliation:MedImmune&s_comma; Emory Vaccine Center&s_comma; Emory University
School of Medicine&s_comma; USA
Seminar Title:Research on herpesvirus vaccines - platforms&s_comma;
immunogenicity and protection -Virus-encoded suppressor of RIP3-RIP1
(Language : English)

Receptor-interacting protein (RIP)3 controls programmed necrosis
(necroptosis)&s_comma; a proinflammatory death pathway distinct from
apoptosis. Murine cytomegalovirus (MCMV)- initiates RIP3-dependent
death during infection. This pathway is suppressed by the viral
inhibitor of RIP activation (vIRA&s_comma; encoded by the M45 gene)&s_comma; a
homotypic interaction motif (RHIM)-containing protein required for
sustained viral infection in cultured cells as well as in mice. vIRA
suppresses necroptosis induced by TNF as well as a RIP3- and TRIF-
dependent death pathway induced by toll-like receptor (TLR)3 and
TLR4. Control of cell death pathways is associated with vIRA RHIM-
dependent disruption of RIP3-RIP1 association&s_comma; a critical upstream
step in necroptosis. Thus&s_comma; MCMV encodes vIRA to specifically block a
RIP3-dependent death pathway common to pathogen recognition and death
receptor engagement. The existence of vIRA validates the importance
of RIP3-dependent death in host defense and adds to the understanding
of how multiple virus-encoded cell death suppressors prevent
premature clearance by different cell death pathways.
スタンフォード大学名誉教授 Edward Mocarski博士が来日されま

Host:Sumiko Watanabe (Division of Molecular and Developmental
Hiroshi Kiyono ( Division of Mucosal Immunology)