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Athena M. Soulika
Researcher at University of California, Davis
Publications - 59
Citations - 2663
Athena M. Soulika is an academic researcher from University of California, Davis. The author has contributed to research in topics: Experimental autoimmune encephalomyelitis & Myelin oligodendrocyte glycoprotein. The author has an hindex of 25, co-authored 55 publications receiving 2190 citations. Previous affiliations of Athena M. Soulika include Fox Chase Cancer Center & Shriners Hospitals for Children.
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Journal ArticleDOI
Glycoprotein D of herpes simplex virus (HSV) binds directly to HVEM, a member of the tumor necrosis factor receptor superfamily and a mediator of HSV entry
J C Whitbeck,Charline Peng,Huan Lou,Ruliang Xu,Sharon H. Willis,M Ponce de Leon,Tao Peng,Anthony V. Nicola,R I Montgomery,M S Warner,Athena M. Soulika,Lynn A. Spruce,William T. Moore,John D. Lambris,Patricia G. Spear,Gary H. Cohen,Roselyn J. Eisenberg +16 more
TL;DR: HVEM interacts directly with gD, suggesting that HV EM is a receptor for virion gD and that the interaction between these proteins is a step in HSV entry into HVEM-expressing cells.
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The Dynamics of the Skin's Immune System
TL;DR: The defensive components of the skin are discussed and the function of skin-resident immune cells in homeostasis and their role in wound healing are focused on.
Journal Article
Interaction of Vaccinia Virus Complement Control Protein with Human Complement Proteins: Factor I-Mediated Degradation of C3b to iC3b1 Inactivates the Alternative Complement Pathway
TL;DR: The results suggest that the interaction of VCP with C3 is different from that of factor H and CR1 and that VCP-supported first cleavage of C3b by factor I is sufficient to render C3B nonfunctional.
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Interaction of vaccinia virus complement control protein with human complement proteins: Factor I-mediated degradation of C3b to iC3b1 inactivates the alternative complement pathway
TL;DR: In this article, a yeast expression system was used to characterize the interaction of VCP with C3 and C4 and understand the mechanism by which VCP inactivates complement, and compared the biologic activity of the purified protein to that of human factor H and complement receptor 1.
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Initiation and progression of axonopathy in experimental autoimmune encephalomyelitis
TL;DR: The hypothesis that both contact-dependent and paracrine interactions of systemic inflammatory cells with axons and an innate immune-mediated neurodegenerative process contribute to axonal loss in this multiple sclerosis model is supported.