About: MLKL Mediated Necroptosis Accelerates JEV-Induced Neuroinflammation in Mice

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About: MLKL Mediated Necroptosis Accelerates JEV-Induced Neuroinflammation in Mice Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	MLKL Mediated Necroptosis Accelerates JEV-Induced Neuroinflammation in Mice
Creator	Zhang, Ying Zhang, Fanglin Zheng, Xuyang Lei, Yingfeng Fan, Hong Suzuki, Ryosuke Bian, Peiyu Cai, Yanhui Jia, Zhansheng Ye, Chuantao Adachi, Akio Colpitts, Tonya Li, † Zhang, Y Arruda, Luciana Cai, Fan
topic	covid:021af77daa9633d212e816cdbaf9f89240bfa3a0#this
Source	PMC
abstract	Japanese encephalitis virus (JEV) is the most prevalent cause of viral encephalitis in Asia and the western Pacific. Neuronal death caused by JEV infection and inflammation induced cytotoxicity leads to progression and deterioration of Japanese encephalitis (JE). Mixed-lineage kinase domain-like protein (MLKL) mediated necroptosis is a newly discovered pathway of programmed cell death and participates in many inflammatory diseases. In this study, we demonstrated for the first time that necroptosis was involved in the neuronal loss during JE via immune-electron microscopy and immunochemistry. The expression of MLKL in neurons was upregulated in presence of JEV infection in vitro and in vivo. Deletion of MLKL alleviated the progression of JE and decreased the level of inflammatory cytokines in mice model. Taken together, this study provides evidence for the participation of necroptosis in the pathogenesis of JEV infection.
has issue date	2017-02-28(xsd:dateTime)
bibo:doi	10.3389/fmicb.2017.00303
bibo:pmid	28293227
has license	cc-by
sha1sum (hex)	021af77daa9633d212e816cdbaf9f89240bfa3a0
schema:url	https://doi.org/10.3389/fmicb.2017.00303
resource representing a document's title	MLKL Mediated Necroptosis Accelerates JEV-Induced Neuroinflammation in Mice
has PubMed Central identifier	PMC5328978
has PubMed identifier	28293227
schema:publication	Front Microbiol
resource representing a document's body	covid:021af77daa9633d212e816cdbaf9f89240bfa3a0#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/021af77daa9633d212e816cdbaf9f89240bfa3a0
is schema:about of	named entity 'INFLAMMATORY DISEASES' named entity 'MODEL' named entity 'NECROPTOSIS' named entity 'MIXED' named entity 'CYTOKINES' named entity 'PROGRAMMED CELL DEATH' named entity 'PATHWAY' named entity 'LEADS' named entity 'STUDY' named entity 'INFECTION' named entity 'CAUSE' named entity 'PATHOGENESIS' named entity 'PRESENCE OF' named entity 'IMMUNE' named entity 'VIRAL ENCEPHALITIS' named entity 'DEMONSTRATED' named entity 'NECROPTOSIS' named entity 'MICE' named entity 'leads' named entity 'necroptosis' named entity 'pathogenesis' named entity 'programmed cell death' named entity 'level' named entity 'study' named entity 'Neuroinflammation' covid:arg/021af77daa9633d212e816cdbaf9f89240bfa3a0 named entity 'INFLAMMATION' named entity 'MLKL' named entity 'PROGRESSION' named entity 'ELECTRON MICROSCOPY' named entity 'LINEAGE' named entity 'JAPANESE ENCEPHALITIS' named entity 'TIME' named entity 'MEDIATED' named entity 'DELETION' named entity 'IS A' named entity 'LIKE' named entity 'EXPRESSION' named entity 'PROVIDES EVIDENCE FOR' named entity 'NEURONS' named entity 'PREVALENT' named entity 'KINASE DOMAIN' named entity 'NEURONAL DEATH' named entity 'MICE' named entity 'NEUROINFLAMMATION' named entity 'MLKL' named entity 'INDUCED' named entity 'INDUCED' named entity 'NEURONAL LOSS' named entity 'UPREGULATED' named entity 'PROTEIN ' named entity 'JAPANESE ENCEPHALITIS VIRUS' named entity 'DETERIORATION' named entity 'WESTERN' named entity 'LEVEL' named entity 'IMMUNOCHEMISTRY' named entity 'ACCELERATES' named entity 'MEDIATED' named entity 'CITATION' named entity 'TAKEN' named entity 'INVOLVED' named entity 'IN VITRO' named entity 'INFLAMMATORY' named entity 'CYTOTOXICITY'

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