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Absence of Cytosolic 2-Cys Prx Subtypes I and II Exacerbates TNF-α-Induced Apoptosis via Different Routes

Authors
 Sunmi Lee  ;  Joo Young Lee  ;  Eun Woo Lee  ;  Sujin Park  ;  Dong Hoon Kang  ;  Chengchun Min  ;  Doo Jae Lee  ;  Dongmin Kang  ;  Jaewhan Song  ;  Jongbum Kwon  ;  Sang Won Kang 
Citation
 CELL REPORTS, Vol.26(8) : 2194-2211, 2019-02 
Journal Title
CELL REPORTS
Issue Date
2019-02
MeSH
3T3 Cells ; Animals ; Apoptosis* ; DNA Damage ; HEK293 Cells ; HeLa Cells ; Histones / metabolism ; Homeodomain Proteins / genetics ; Homeodomain Proteins / metabolism* ; Humans ; Hydrogen Peroxide / toxicity ; Inhibitor of Apoptosis Proteins / metabolism ; MCF-7 Cells ; Mice ; Mice, Inbred BALB C ; Oxidative Stress ; Receptor-Interacting Protein Serine-Threonine Kinases / metabolism ; Tumor Necrosis Factor-alpha / metabolism ; Ubiquitin-Protein Ligases / metabolism
Keywords
DNA damage ; H(2)O(2) ; RIPK1 ; TNF-α ; apoptosis ; cIAP ; peroxiredoxin
Abstract
There are abundant peroxiredoxin (Prx) enzymes, but an increase of cellular H2O2 level always happens in apoptotic cells. Here, we show that cellular H2O2 switches different apoptosis pathways depending on which type of Prx enzyme is absent. TNF alpha-induced H2O2 burst preferentially activates the DNA damage-dependent apoptosis pathway in the absence of PrxI. By contrast, the same H2O2 burst stimulates the RIPK1-dependent apoptosis pathway in the absence of PrxII by inducing the destruction of cIAP1 in caveolar membrane. Specifically, H2O2 induces the oxidation of Cys308 residue in the cIAP1-BIR3 domain, which induces the dimerization-dependent E3 ligase activation. Thus, the reduction in cIAP level by the absence of PrxII triggers cell-autonomous apoptosis in cancer cells and tumors. Such differential functions of PrxI and PrxII are mediated by interaction with H2AX and cIAP1, respectively. Collectively, this study reveals the distinct switch roles of 2-Cys Prx isoforms in apoptosis signaling.
Files in This Item:
T9992019124.pdf Download
DOI
10.1016/j.celrep.2019.01.081
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Lee, Joo Young(이주영)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/189127
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