Characterization and function of mandarin fish c-Myc during viral infection process

Author(s):  
Caimei Ye ◽  
Li Ningqiu ◽  
Niu Yinjie ◽  
Lin Qiang ◽  
Luo Xia ◽  
...  
Cell Reports ◽  
2020 ◽  
Vol 31 (13) ◽  
pp. 107827 ◽  
Author(s):  
Kristen E. Pauken ◽  
Jernej Godec ◽  
Pamela M. Odorizzi ◽  
Keturah E. Brown ◽  
Kathleen B. Yates ◽  
...  

2017 ◽  
Vol 67 (2) ◽  
pp. 214-227.e7 ◽  
Author(s):  
Xiang Li ◽  
Chu-Xiao Liu ◽  
Wei Xue ◽  
Yang Zhang ◽  
Shan Jiang ◽  
...  
Keyword(s):  

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Yuanzhi Liu ◽  
Mingshu Wang ◽  
Anchun Cheng ◽  
Qiao Yang ◽  
Ying Wu ◽  
...  

Abstract Background eIF2α is a regulatory node that controls protein synthesis initiation by its phosphorylation or dephosphorylation. General control nonderepressible-2 (GCN2), protein kinase R-like endoplasmic reticulum kinase (PERK), double-stranded RNA (dsRNA)-dependent protein kinase (PKR) and heme-regulated inhibitor (HRI) are four kinases that regulate eIF2α phosphorylation. Main body In the viral infection process, dsRNA or viral proteins produced by viral proliferation activate different eIF2α kinases, resulting in eIF2α phosphorylation, which hinders ternary tRNAMet-GTP-eIF2 complex formation and inhibits host or viral protein synthesis. The stalled messenger ribonucleoprotein (mRNP) complex aggregates under viral infection stress to form stress granules (SGs), which encapsulate viral RNA and transcription- and translation-related proteins, thereby limiting virus proliferation. However, many viruses have evolved a corresponding escape mechanism to synthesize their own proteins in the event of host protein synthesis shutdown and SG formation caused by eIF2α phosphorylation, and viruses can block the cell replication cycle through the PERK-eIF2α pathway, providing a favorable environment for their own replication. Subsequently, viruses can induce host cell autophagy or apoptosis through the eIF2α-ATF4-CHOP pathway. Conclusions This review summarizes the role of eIF2α in viral infection to provide a reference for studying the interactions between viruses and hosts.


Glycosciences ◽  
2008 ◽  
pp. 245-259 ◽  
Author(s):  
Werner Reutter ◽  
Roger Stsche ◽  
Peer Stehling ◽  
Oliver Baum

2004 ◽  
Vol 286 (2) ◽  
pp. L388-L398 ◽  
Author(s):  
Rommel S. Lan ◽  
Geoffrey A. Stewart ◽  
Roy G. Goldie ◽  
Peter J. Henry

Protease-activated receptors (PARs) are widely distributed in human airways, and recent evidence indicates a role for PARs in the pathophysiology of inflammatory airway disease. To further investigate the role of PARs in airway disease, we determined the expression and function of PARs in a murine model of respiratory tract viral infection. PAR-1, PAR-2, PAR-3, and PAR-4 mRNA and protein were expressed in murine airways, and confocal microscopy revealed colocalization of PAR-2 and cyclooxygenase (COX)-2 immunostaining in basal tracheal epithelial cells. Elevated levels of PAR immunostaining, which was particularly striking for PAR-1 and PAR-2, were observed in the airways of influenza A/PR-8/34 virus-infected mice compared with sham-infected mice. Furthermore, increased PAR-1 and PAR-2 expression was associated with significant changes in in vivo lung function responses. PAR-1 agonist peptide potentiated methacholine-induced increases in airway resistance in anesthetized sham-infected mice (and in indomethacin-treated, virus-infected mice), but no such potentiation was observed in virus-infected mice. PAR-2 agonist peptide transiently inhibited methacholine-induced bronchoconstriction in sham-infected mice, and this effect was prolonged in virus-infected mice. These findings suggest that during viral infection, the upregulation of PARs in the airways is coupled to increased activation of COX and enhanced generation of bronchodilatory prostanoids.


2021 ◽  
Vol 8 ◽  
Author(s):  
Peng Hu ◽  
Bingxia Ming ◽  
Xuefen Wu ◽  
Shaozhe Cai ◽  
Jungen Tang ◽  
...  

Evidences have suggested that Sjogren's syndrome (SS) is associated with viral infection. The aim of this study was to investigate the involvement of respiratory viral poly(I:C) in the pathogenesis of SS and potential mechanisms using a SS-like NOD/ShiLtJ (NOD) mouse model. 5-week female NOD mice were intratracheally administered poly(I:C) every other day for 5 times to mimic viral infection. Pilocarpine induced saliva secretion was determined every 8 days. Submandibular glands (SMG) and lungs were harvested for the detection of pathological changes. We found that intratracheal administration of poly(I:C) significantly advanced and enhanced the reduction of saliva flow rate in NOD mice. Furthermore, poly(I:C) treatment aggravated the histopathological lesions and inflammatory cells infiltration in SMG. Accompanied by elevated expression of IFN cytokines and IL-33, Th1 activation was enhanced in SMG of poly(I:C)-treated NOD mice, but Th17 cells activation was unchanged among the groups. In addition, intratracheal poly(I:C) exposure promoted the expression of IL-33 and increased T cells proportion in the lung, which were consistent with the change in SMG. Therefore, intratracheal poly(I:C) exposure aggravated the immunological and function disorder of SMG in NOD mice.


2004 ◽  
Vol 68 (3) ◽  
pp. 432-452 ◽  
Author(s):  
Qiaoqiao Wang ◽  
Gordon G. Carmichael

SUMMARY Since double-stranded RNA (dsRNA) has not until recently generally been thought to be deliberately expressed in cells, it has commonly been assumed that the major source of cellular dsRNA is viral infections. In this view, the cellular responses to dsRNA would be natural and perhaps ancient antiviral responses. While the cell may certainly react to some dsRNAs as an antiviral response, this does not represent the only response or even, perhaps, the major one. A number of recent observations have pointed to the possibility that dsRNA molecules are not seen only as evidence of viral infection or recognized for degradation because they cannot be translated. In some instances they may also play important roles in normal cell growth and function. The purpose of this review is to outline our current understanding of the fate of dsRNA in cells, with a focus on the apparent fact that their fates and functions appear to depend critically not only on where in the cell dsRNA molecules are found, but also on how long they are and perhaps on how abundant they are.


2010 ◽  
Vol 03 (01) ◽  
pp. 1-19 ◽  
Author(s):  
ZHI XIE ◽  
DON KULASIRI

Intrinsic and extrinsic noises are all believed to be important in the development and function of many living organisms. In this study, we investigate the sources of the intrinsic noise and the influence of the extrinsic noise on an intracellular viral infection system. The contribution of the intrinsic noise from each reaction is measured by means of a special form of stochastic differential equations (SDEs), chemical Langevin equation. The intrinsic noise of the system is a linear sum of the noise in each of the reactions. The intrinsic noise mainly arises from the degradation of mRNA and the transcription processes. We then study the effects of extrinsic noise by the means of a general form of SDE. It is found that the noise of the viral components grows logarithmically with the increasing noise intensities. The system is most susceptible to the noise in the virus assembly process. A high level of noise in this process can even inhibit the growth of the viruses. This study also demonstrates the utility of SDEs in analyzing genetic regulatory networks perturbed by either inherent or parametric stochasticity.


2019 ◽  
Vol 20 (22) ◽  
pp. 5602 ◽  
Author(s):  
Yawei Shen ◽  
Ziwei Zhao ◽  
Jinliang Zhao ◽  
Xiaowu Chen ◽  
Ming Cao ◽  
...  

Hepcidin is a liver-derived peptide hormone that is related to iron balance and immunity in humans. However, its function in Siniperca chuatsi has not been well elucidated. In this study, we analyzed the expression and function of the S. chuatsi hepcidin (Sc-hep) gene. Sc-hep was specifically expressed in the liver and appeared to be one of the most highly expressed genes in the liver. After spleen and kidney necrosis virus (ISKNV) infection and lipopolysaccharide (LPS) and polyinosinic—polycytidylic acid (Poly I:C) stimulation, the expression of Sc-hep in the liver increased by approximately 110, 6500, and 225 times, respectively. After ferrous sulfate (FS) injection, the expression of Sc-hep in the liver increased approximately 520-fold. We found that miR-19c-5p could inhibit Sc-hep expression. Five CpG dinucleotides distributed in the promoter region showed no differential methylation between the liver and the stomach, both presenting high methylation rates. After FS or LPS injection, the expression of three iron balance-related genes (FPN1, TFR1, and FTN) and five immune-related cytokine genes (IL-1β, IL8, TNF-α, TLR22, and SOCS3) significantly changed. These results indicate that Sc-hep participates in the regulation of iron balance and plays an important role in the immune system. Sc-hep increased approximately 52-fold when mandarin fish were domesticated with artificial diets. Sc-hep might be used as a real-time biomarker of mandarin fish liver because its expression markedly varies under different physiological conditions.


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