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O-GlcNAcylation of RIPK1 rescues red blood cells from necroptosis

Authors
 Junghwa Seo  ;  Yeolhoe Kim  ;  Suena Ji  ;  Han Byeol Kim  ;  Hyeryeon Jung  ;  Eugene C Yi  ;  Yong-Ho Lee  ;  Injae Shin  ;  Won Ho Yang  ;  Jin Won Cho 
Citation
 FRONTIERS IN IMMUNOLOGY, Vol.14 : 1160490, 2023-06 
Journal Title
FRONTIERS IN IMMUNOLOGY
Issue Date
2023-06
MeSH
Animals ; Apoptosis* / physiology ; Erythrocytes / metabolism ; Humans ; Mice ; Necroptosis* ; Necrosis ; Receptor-Interacting Protein Serine-Threonine Kinases / genetics ; Receptor-Interacting Protein Serine-Threonine Kinases / metabolism ; Serine
Keywords
O-GlcNAcylation ; erythrocyte ; necroptosis ; receptor interacting protein kinase1 (RIPK1) ; red blood cell
Abstract
Necroptosis is a type of cell death with excessive inflammation and organ damage in various human diseases. Although abnormal necroptosis is common in patients with neurodegenerative, cardiovascular, and infectious diseases, the mechanisms by which O-GlcNAcylation contributes to the regulation of necroptotic cell death are poorly understood. In this study, we reveal that O-GlcNAcylation of RIPK1 (receptor-interacting protein kinase1) was decreased in erythrocytes of the mouse injected with lipopolysaccharide, resulting in the acceleration of erythrocyte necroptosis through increased formation of RIPK1-RIPK3 complex. Mechanistically, we discovered that O-GlcNAcylation of RIPK1 at serine 331 in human (corresponding to serine 332 in mouse) inhibits phosphorylation of RIPK1 at serine 166, which is necessary for the necroptotic activity of RIPK1 and suppresses the formation of the RIPK1-RIPK3 complex in Ripk1 -/- MEFs. Thus, our study demonstrates that RIPK1 O-GlcNAcylation serves as a checkpoint to suppress necroptotic signaling in erythrocytes.
Files in This Item:
T202303698.pdf Download
DOI
10.3389/fimmu.2023.1160490
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Seo, Jung Hwa(서정화)
Lee, Yong Ho(이용호) ORCID logo https://orcid.org/0000-0002-6219-4942
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/195565
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