Inhibition of O-GlcNAcylation protects from Shiga toxin-mediated cell injury and lethality in host
DC Field | Value | Language |
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dc.contributor.author | Lee, Kyung-Soo | - |
dc.contributor.author | Lee, Jieun | - |
dc.contributor.author | Lee, Pureum | - |
dc.contributor.author | Jeon, Bong Chan | - |
dc.contributor.author | Song, Min Yeong | - |
dc.contributor.author | Kwak, Sojung | - |
dc.contributor.author | Lee, Jungwoon | - |
dc.contributor.author | Kim, Jun-Seob | - |
dc.contributor.author | Kim, Doo-Jin | - |
dc.contributor.author | Kim, Ji Hyung | - |
dc.contributor.author | Tesh, Vernon L. | - |
dc.contributor.author | Lee, Moo-Seung | - |
dc.contributor.author | Park, Sung-Kyun | - |
dc.date.accessioned | 2022-06-10T02:40:08Z | - |
dc.date.available | 2022-06-10T02:40:08Z | - |
dc.date.created | 2022-06-10 | - |
dc.date.issued | 2022-01 | - |
dc.identifier.issn | 1757-4676 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/84592 | - |
dc.description.abstract | Shiga toxins (Stxs) produced by enterohemorrhagic Escherichia coli (EHEC) are the major virulence factors responsible for hemorrhagic colitis, which can lead to life-threatening systemic complications including acute renal failure (hemolytic uremic syndrome) and neuropathy. Here, we report that O-GlcNAcylation, a type of post-translational modification, was acutely increased upon induction of endoplasmic reticulum (ER) stress in host cells by Stxs. Suppression of the abnormal Stx-mediated increase in O-GlcNAcylation effectively inhibited apoptotic and inflammatory responses in Stx-susceptible cells. The protective effect of O-GlcNAc inhibition for Stx-mediated pathogenic responses was also verified using three-dimensional (3D)-cultured spheroids or organoids mimicking the human kidney. Treatment with an O-GlcNAcylation inhibitor remarkably improved the major disease symptoms and survival rate for mice intraperitoneally injected with a lethal dose of Stx. In conclusion, this study elucidates O-GlcNAcylation-dependent pathogenic mechanisms of Stxs and demonstrates that inhibition of aberrant O-GlcNAcylation is a potential approach to treat Stx-mediated diseases. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.relation.isPartOf | EMBO MOLECULAR MEDICINE | - |
dc.title | Inhibition of O-GlcNAcylation protects from Shiga toxin-mediated cell injury and lethality in host | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000723194200001 | - |
dc.identifier.doi | 10.15252/emmm.202114678 | - |
dc.identifier.bibliographicCitation | EMBO MOLECULAR MEDICINE, v.14, no.1 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.scopusid | 2-s2.0-85120062486 | - |
dc.citation.title | EMBO MOLECULAR MEDICINE | - |
dc.citation.volume | 14 | - |
dc.citation.number | 1 | - |
dc.contributor.affiliatedAuthor | Kim, Ji Hyung | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | hemolytic uremic syndrome | - |
dc.subject.keywordAuthor | inflammation | - |
dc.subject.keywordAuthor | O-GlcNAcylation | - |
dc.subject.keywordAuthor | Shiga toxin | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | BETA-N-ACETYLGLUCOSAMINE | - |
dc.subject.keywordPlus | GLCNAC MODIFICATION | - |
dc.subject.keywordPlus | CROSS-TALK | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | MODEL | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | GLUCOSAMINE | - |
dc.subject.keywordPlus | METABOLISM | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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