About: eIF2α-CHOP-BCl-2/JNK and IRE1α-XBP1/JNK signaling promote apoptosis and inflammation and support the proliferation of Newcastle disease virus

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About: eIF2α-CHOP-BCl-2/JNK and IRE1α-XBP1/JNK signaling promote apoptosis and inflammation and support the proliferation of Newcastle disease virus 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	eIF2α-CHOP-BCl-2/JNK and IRE1α-XBP1/JNK signaling promote apoptosis and inflammation and support the proliferation of Newcastle disease virus
Creator	Ding, Chan Jiang, Weiyu Li, Yanrong Liao, Ying Meng, Chunchun Niu, Qiaona Qiu, Xusheng Song, Cuiping Sun, Yingjie Tan, Lei
Source	PMC
abstract	Newcastle disease virus (NDV) causes severe infectious disease in poultry and selectively kills tumor cells, by inducing apoptosis and cytokines secretion. In this report, we study the mechanisms underlying NDV-induced apoptosis by investigating the unfolded protein response (UPR). We found that NDV infection activated all three branches of the UPR signaling (PERK-eIF2α, ATF6, and IRE1α) and triggered apoptosis, in avian cells (DF-1 and CEF) and in various human cancer cell types (HeLa, Cal27, HN13, A549, H1299, Huh7, and HepG2). Interestingly, the suppression of either apoptosis or UPR led to impaired NDV proliferation. Meanwhile, the inhibition of UPR by 4-PBA protected cells from NDV-induced apoptosis. Further study revealed that activation of PERK-eIF2α induced the expression of transcription factor CHOP, which subsequently promoted apoptosis by downregulating BCL-2/MCL-1, promoting JNK signaling and suppressing AKT signaling. In parallel, IRE1α mediated the splicing of XBP1 mRNA and resulted in the translation and nuclear translocation of XBP1s, thereby promoting the transcription of ER chaperones and components of ER-associated degradation (ERAD). Furthermore, IRE1α promoted apoptosis and cytokines secretion via the activation of JNK signaling. Knock down and overexpression studies showed that CHOP, IRE1α, XBP1, and JNK supported efficient virus proliferation. Our study demonstrates that the induction of eIF2α-CHOP-BCL-2/JNK and IRE1α-XBP1/JNK signaling cascades promote apoptosis and cytokines secretion, and these signaling cascades support NDV proliferation.
has issue date	2019-11-26(xsd:dateTime)
bibo:doi	10.1038/s41419-019-2128-6
bibo:pmid	31767828
has license	cc-by
sha1sum (hex)	85bab4f8869727adbe47f5ddc6e18af508dc57a0
schema:url	https://doi.org/10.1038/s41419-019-2128-6
resource representing a document's title	eIF2α-CHOP-BCl-2/JNK and IRE1α-XBP1/JNK signaling promote apoptosis and inflammation and support the proliferation of Newcastle disease virus
has PubMed Central identifier	PMC6877643
has PubMed identifier	31767828
schema:publication	Cell Death Dis
resource representing a document's body	covid:85bab4f8869727adbe47f5ddc6e18af508dc57a0#body_text
is schema:about of	covid:arg/85bab4f8869727adbe47f5ddc6e18af508dc57a0 named entity 'cancer cell' named entity 'apoptosis' named entity 'NDV' named entity 'XBP1' named entity 'NDV' named entity 'Huh7' named entity 'chaperones' named entity 'apoptosis' named entity 'mRNA' named entity 'HeLa' named entity 'apoptosis' named entity 'apoptosis' named entity 'IRE1α' named entity 'transcription factor' named entity 'virus' named entity 'BCL-2' named entity 'cytokines' named entity 'signaling cascades' named entity 'NDV' named entity 'splicing' named entity 'apoptosis' named entity 'eIF2α' named entity 'IRE1α' named entity 'inflammation' named entity 'Newcastle disease' named entity 'H1299' named entity 'NDV' named entity 'Huh7' named entity 'ligated' named entity 'NDV' named entity 'apoptosis' named entity 'phosphorylation' named entity 'HeLa' named entity 'serially diluted' named entity 'eIF2α' named entity 'NDV' named entity 'Immunofluorescence' named entity 'virus' named entity 'BAX' named entity 'XBP1' named entity 'JNK' named entity 'Denmark' named entity 'HeLa cells' named entity 'apoptosis' named entity 'pro-apoptotic' named entity 'PERK' named entity 'XBP1' named entity 'reverse transcriptase' named entity 'translational machinery' named entity 'lumen' named entity 'apoptosis' named entity 'IRE1α' named entity 'HepG2' named entity 'eIF2-GTP' named entity 'JNK' named entity 'JNK' named entity 'innate immune response' named entity 'DF-1' named entity 'antibody' named entity 'NDV' named entity 'UPR' named entity 'p38' named entity 'protein' named entity 'Bio-Rad' named entity 'cell growth' named entity 'lumen' named entity 'PERK' named entity 'cell culture medium' named entity 'staining' named entity 'PUMA' named entity 'PERK'

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