Upregulation of CHOP/GADD153 during Coronavirus Infectious Bronchitis Virus Infection Modulates Apoptosis by Restricting Activation of the Extracellular Signal-Regulated Kinase Pathway

Liao, Ying; Fung, To Sing; Huang, Mei; Fang, Shou Guo; Zhong, Yanxin; Liu, Ding Xiang

doi:10.1128/jvi.00626-13

Cited by 113 publications

(133 citation statements)

References 66 publications

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“…Consistent with these findings, activation of luciferase reporters under the control of BiP or GRP94 promoters has been observed in cells infected with SARS-CoV (Chan et al, 2006). ER stress has also been observed in cells infected with other coronaviruses such as MHV (Versteeg et al, 2007) or IBV (Liao et al, 2013). Therefore, ER stress induction is likely a common outcome in cells infected with coronaviruses .…”

Section: Induction Of Er Stress By Coronavirus Infectionsupporting

confidence: 68%

“…The effective inhibition of PKR (and likely also PERK) phosphorylation has been attributed to the nsp2 protein, which dosage dependently restore the PKR-mediated translation suppression of a reporter construct (Wang et al, 2009). The kinetic of eIF2␣ phosphorylation is similar to that of PKR and PERK, which peaks at early infection but drastically reduces afterwards (Liao et al, 2013;Wang et al, 2009). As a result, de novo synthesis of host proteins is not significantly suppressed in IBV-infected cells throughout the course of infection (Wang et al, 2009).…”

Section: Activation Of Isr During Coronavirus Infectionmentioning

confidence: 85%

“…In terms of Gammacoronaviruses, studies done by this group have shown that IBV triggers phosphorylation of PKR and PERK at early time points of infection (2-8 hpi), which diminished quickly thereafter (Liao et al, 2013;Wang et al, 2009). The effective inhibition of PKR (and likely also PERK) phosphorylation has been attributed to the nsp2 protein, which dosage dependently restore the PKR-mediated translation suppression of a reporter construct (Wang et al, 2009).…”

Section: Activation Of Isr During Coronavirus Infectionmentioning

confidence: 99%

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Coronavirus-induced ER stress response and its involvement in regulation of coronavirus–host interactions

2014

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Coronavirus replication is structurally and functionally associated with the endoplasmic reticulum (ER), a major site of protein synthesis, folding, modification and sorting in the eukaryotic cells. Disturbance of ER homeostasis may occur under various physiological or pathological conditions. In response to the ER stress, signaling pathways of the unfolded protein response (UPR) are activated. UPR is mediated by three ER transmembrane sensors, namely the PKR-like ER protein kinase (PERK), the inositol-requiring protein 1 (IRE1) and the activating transcriptional factor 6 (ATF6). UPR facilitates adaptation to ER stress by reversible translation attenuation, enhancement of ER protein folding capacity and activation of ER-associated degradation (ERAD). In cells under prolonged and irremediable ER stress, UPR can also trigger apoptotic cell death. Accumulating evidence has shown that coronavirus infection causes ER stress and induces UPR in the infected cells. UPR is closely associated with a number of major signaling pathways, including autophagy, apoptosis, the mitogen-activated protein (MAP) kinase pathways, innate immunity and pro-inflammatory response. Therefore, studies on the UPR are pivotal in elucidating the complicated issue of coronavirus-host interaction. In this paper, we present the up-to-date knowledge on coronavirus-induced UPR and discuss its potential involvement in regulation of innate immunity and apoptosis.

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Section: Induction Of Er Stress By Coronavirus Infectionsupporting

confidence: 68%

Section: Activation Of Isr During Coronavirus Infectionmentioning

confidence: 85%

Section: Activation Of Isr During Coronavirus Infectionmentioning

confidence: 99%

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Coronavirus-induced ER stress response and its involvement in regulation of coronavirus–host interactions

2014

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“…Minakshi et al analyzed this by transfecting Huh7 cells with p3a and luciferase-tagged ER stress-related molecules, showing that it can enhance protein folding, but not activate Endoplasmic Reticulum Associated Degradation (ERAD) Minakshi et al, 2009. The long-term triggering of the PERK pathway can also induce virus-related apoptosis through the expression of its downstream mediators of ATF4 and CHOP, similar to IBV infection (Liao et al, 2013). Padhan et al have shown that protein 3a can lead to increased activation of the p38 MAP kinase pathway and induce the mitochondria to leak cytochrome c to induce apoptosis (Padhan et al, 2008).…”

Section: Sars-cov P3amentioning

confidence: 99%

Accessory proteins of SARS-CoV and other coronaviruses

et al. 2014

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The huge RNA genome of SARS coronavirus comprises a number of open reading frames that code for a total of eight accessory proteins. Although none of these are essential for virus replication, some appear to have a role in virus pathogenesis. Notably, some SARS-CoV accessory proteins have been shown to modulate the interferon signaling pathways and the production of pro-inflammatory cytokines. The structural information on these proteins is also limited, with only two (p7a and p9b) having their structures determined by X-ray crystallography. This review makes an attempt to summarize the published knowledge on SARS-CoV accessory proteins, with an emphasis on their involvement in virus-host interaction. The accessory proteins of other coronaviruses are also briefly discussed. This paper forms part of a series of invited articles in Antiviral Research on "From SARS to MERS: 10 years of research on highly pathogenic human coronaviruses" (see Introduction by Hilgenfeld and Peiris (2013)).

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“…Moreover, GADD153 and c-myc are known to be involved in apoptosis progression. GADD153 is a member of the CCAAT/ enhancer-binding protein family of transcription factors and its expression is markedly enhanced by various cellular stresses (22,23). On the other hand, c-myc is a proto-oncogene and is implicated in various processes including cell growth, proliferation and cell death (24).…”

Section: Discussionmentioning

confidence: 99%

Effect of Celergen, a marine derivative, on in vitro hepatocarcinogenesis

Catanzaro¹,

Zerbinati²,

Solimene

et al. 2013

Drug Discov Ther

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The aim of this study was to test for a potential anticarcinogenic effect of Celergen, a marine derivative devoid of traceable amounts of inorganic arsenic, on cell proliferation, cell cycle progression and apoptosis in the HepG2 human liver cancer cell line. Celergen significantly inhibited the proliferation of cancer cells in a dose-dependent manner while limiting the cell cycle progression at the G1 phase and significantly inducing apoptosis. Further examination showed that Celergen enhanced expression of the p21 CIPl1WAF1 , GADD153 genes and downregulated the c-myc gene. These results suggest that Celergen exerts promising chemopreventive properties to be further investigated.

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Upregulation of CHOP/GADD153 during Coronavirus Infectious Bronchitis Virus Infection Modulates Apoptosis by Restricting Activation of the Extracellular Signal-Regulated Kinase Pathway

Cited by 113 publications

References 66 publications

Coronavirus-induced ER stress response and its involvement in regulation of coronavirus–host interactions

Coronavirus-induced ER stress response and its involvement in regulation of coronavirus–host interactions

Accessory proteins of SARS-CoV and other coronaviruses

Effect of Celergen, a marine derivative, on in vitro hepatocarcinogenesis

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