Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.isci.2021.103514
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dc.titleToxoplasma gondii SAG1 targeting host cell S100A6 for parasite invasion and host immunity
dc.contributor.authorZhou, Li-Juan
dc.contributor.authorPeng, Jiao
dc.contributor.authorChen, Min
dc.contributor.authorYao, Li-Jie
dc.contributor.authorZou, Wei-Hao
dc.contributor.authorHe, Cynthia Y.
dc.contributor.authorPeng, Hong-Juan
dc.date.accessioned2022-10-13T01:03:23Z
dc.date.available2022-10-13T01:03:23Z
dc.date.issued2021-11-01
dc.identifier.citationZhou, Li-Juan, Peng, Jiao, Chen, Min, Yao, Li-Jie, Zou, Wei-Hao, He, Cynthia Y., Peng, Hong-Juan (2021-11-01). Toxoplasma gondii SAG1 targeting host cell S100A6 for parasite invasion and host immunity. iScience 24 (12) : 103514. ScholarBank@NUS Repository. https://doi.org/10.1016/j.isci.2021.103514
dc.identifier.issn2589-0042
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/232671
dc.description.abstractToxoplasma gondii surface antigen 1 (TgSAG1) is a surface protein of tachyzoites, which plays a crucial role in toxoplasma gondii infection and host cell immune regulation. However, how TgSAG1 regulates these processes remains elucidated. We utilized the biotin ligase -TurboID fusion with TgSAG1 to identify the host proteins interacting with TgSAG1, and identified that S100A6 was co-localized with TgSAG1 when T. gondii attached to the host cell. S100A6, either knocking down or blocking its functional epitopes resulted in inhibited parasites invasion. Meanwhile, S100A6 overexpression in host cells promoted T. gondii infection. We further verified that TgSAG1 could inhibit the interaction of host cell vimentin with S100A6 for cytoskeleton organization during T. gondii invasion. As an immunogen, TgSAG1 could promote the secretion of tumor necrosis factor alpha (TNF-?) through S100A6-Vimentin/PKC?-NF-?B signaling pathway. In summary, our findings revealed a mechanism for how TgSAG1 functioned in parasitic invasion and host immune regulation. © 2021
dc.publisherElsevier Inc.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.sourceScopus OA2021
dc.subjectImmune response
dc.subjectMolecular biology
dc.subjectParasitology
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1016/j.isci.2021.103514
dc.description.sourcetitleiScience
dc.description.volume24
dc.description.issue12
dc.description.page103514
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