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Coxsackievirus B3 replication and pathogenesis.
Garmaroudi FS, Marchant D, Hendry R, Luo H, Yang D, Ye X, Shi J, McManus BM. Garmaroudi FS, et al. Among authors: yang d. Future Microbiol. 2015;10(4):629-53. doi: 10.2217/fmb.15.5. Future Microbiol. 2015. PMID: 25865198 Free article. Review.
Evolution has equipped this pico-rna-virus, CVB3, to use different strategies, including CVB3-induced direct damage to host cells followed by a host inflammatory response to CVB3 infection, and cell death to super-additively promote target organ tissue injury …
Evolution has equipped this pico-rna-virus, CVB3, to use different strategies, including CVB3-induced direct damage to host ce …
Expression Profile and Function Analysis of Long Non-coding RNAs in the Infection of Coxsackievirus B3.
Tong L, Qiu Y, Wang H, Qu Y, Zhao Y, Lin L, Wang Y, Xu W, Zhao W, He H, Zhao G, Zhang MH, Yang D, Ge X, Zhong Z. Tong L, et al. Among authors: yang d. Virol Sin. 2019 Dec;34(6):618-630. doi: 10.1007/s12250-019-00152-x. Epub 2019 Aug 6. Virol Sin. 2019. PMID: 31388922 Free PMC article.
According to lncRNA-mRNA correlation, we found that XLOC-001188, an lncRNA down-regulated in CVB3 infection, was negatively correlated with NFAT5 mRNA, an anti-CVB3 gene reported previously. ...In all, our studies reveal the alteration of lncRNA expression in CVB
According to lncRNA-mRNA correlation, we found that XLOC-001188, an lncRNA down-regulated in CVB3 infection, was negatively correlate …
The impact of CVB3 infection on host cell biology.
Marchant D, Si X, Luo H, McManus B, Yang D. Marchant D, et al. Among authors: yang d. Curr Top Microbiol Immunol. 2008;323:177-98. doi: 10.1007/978-3-540-75546-3_8. Curr Top Microbiol Immunol. 2008. PMID: 18357770 Review.
CVB3 myocarditis can lead to dilated cardiomyopath (DCM). DCM is one of the leading causes of the need for heart transplantation, so it is important to understand the life cycle of CVB3 and its interactions with the host cell. ...Interactions of host cell proteins w
CVB3 myocarditis can lead to dilated cardiomyopath (DCM). DCM is one of the leading causes of the need for heart transplantation, so
Cleavage of osmosensitive transcriptional factor NFAT5 by Coxsackieviral protease 2A promotes viral replication.
Qiu Y, Ye X, Zhang HM, Hanson P, Zhao G, Tong L, Xie R, Yang D. Qiu Y, et al. Among authors: yang d. PLoS Pathog. 2017 Dec 8;13(12):e1006744. doi: 10.1371/journal.ppat.1006744. eCollection 2017 Dec. PLoS Pathog. 2017. PMID: 29220410 Free PMC article.
The necessity of iNOS for the anti-CVB3 effect of NFAT5 was supported by the observation that inhibition of iNOS blocked the anti-CVB3 effect of NFAT5. ...Taken together, our data demonstrate that the anti-CVB3 activity of NFAT5 is impaired during CVB3
The necessity of iNOS for the anti-CVB3 effect of NFAT5 was supported by the observation that inhibition of iNOS blocked the anti- …
Cleavage and Sub-Cellular Redistribution of Nuclear Pore Protein 98 by Coxsackievirus B3 Protease 2A Impairs Cardioprotection.
Hanson PJ, Hossain AR, Qiu Y, Zhang HM, Zhao G, Li C, Lin V, Sulaimon S, Vlok M, Fung G, Chen VH, Jan E, McManus BM, Granville DJ, Yang D. Hanson PJ, et al. Among authors: yang d. Front Cell Infect Microbiol. 2019 Jul 24;9:265. doi: 10.3389/fcimb.2019.00265. eCollection 2019. Front Cell Infect Microbiol. 2019. PMID: 31396490 Free PMC article.
NUP98 was cleaved as early as 2 h post-CVB3 infection. This cleavage was further verified through both the ectopic expression of viral proteases and in vitro using purified recombinant CVB3 proteases (2A and 3C), which demonstrated that CVB3 2A but not 3C is …
NUP98 was cleaved as early as 2 h post-CVB3 infection. This cleavage was further verified through both the ectopic expression of vira …
Hsp70-1: upregulation via selective phosphorylation of heat shock factor 1 during coxsackieviral infection and promotion of viral replication via the AU-rich element.
Qiu Y, Ye X, Hanson PJ, Zhang HM, Zong J, Cho B, Yang D. Qiu Y, et al. Among authors: yang d. Cell Mol Life Sci. 2016 Mar;73(5):1067-84. doi: 10.1007/s00018-015-2036-6. Epub 2015 Sep 11. Cell Mol Life Sci. 2016. PMID: 26361762
Coxsackievirus B3 (CVB3) is the primary pathogen of viral myocarditis. Upon infection, CVB3 exploits the host cellular machineries, such as chaperone proteins, to benefit its own infection cycles. ...Finally, we demonstrated that Hsp70-1 upregulation, in turn, stabi …
Coxsackievirus B3 (CVB3) is the primary pathogen of viral myocarditis. Upon infection, CVB3 exploits the host cellular machine …
Involvement of Endoplasmic Reticulum Stress-Mediated C/EBP Homologous Protein Activation in Coxsackievirus B3-Induced Acute Viral Myocarditis.
Cai Z, Shen L, Ma H, Yang J, Yang D, Chen H, Wei J, Lu Q, Wang DW, Xiang M, Wang J. Cai Z, et al. Among authors: yang d. Circ Heart Fail. 2015 Jul;8(4):809-18. doi: 10.1161/CIRCHEARTFAILURE.114.001244. Epub 2015 May 18. Circ Heart Fail. 2015. PMID: 25985795
METHODS AND RESULTS: AVMC was induced by intraperitoneal injection of 1000 tissue culture infectious dose (TCID50) of CVB3 virus in mice. ...Strikingly, CHOP deficiency exhibited dramatic protective effects on cardiac damage, cardiac dysfunction, viral replication, and pro …
METHODS AND RESULTS: AVMC was induced by intraperitoneal injection of 1000 tissue culture infectious dose (TCID50) of CVB3 virus in m …
Secondary heterotypic versus homotypic infection by Coxsackie B group viruses: impact on early and late histopathological lesions and virus genome prominence.
Yu JZ, Wilson JE, Wood SM, Kandolf R, Klingel K, Yang D, McManus BM. Yu JZ, et al. Among authors: yang d. Cardiovasc Pathol. 1999 Mar-Apr;8(2):93-102. doi: 10.1016/s1054-8807(98)00025-8. Cardiovasc Pathol. 1999. PMID: 10724506
Seven days after secondary heterotypic (CVB2-CVB3) infection, the quantity of CVB genome in heart, pancreas, liver, and spleen was increased compared with the virus genome in the CVB3-CVB3 group and in the group with primary CVB3 infection alone. ...Vi …
Seven days after secondary heterotypic (CVB2-CVB3) infection, the quantity of CVB genome in heart, pancreas, liver, and spleen was in …
Heat shock protein 70 promotes coxsackievirus B3 translation initiation and elongation via Akt-mTORC1 pathway depending on activation of p70S6K and Cdc2.
Wang F, Qiu Y, Zhang HM, Hanson P, Ye X, Zhao G, Xie R, Tong L, Yang D. Wang F, et al. Among authors: yang d. Cell Microbiol. 2017 Jul;19(7). doi: 10.1111/cmi.12725. Epub 2017 Feb 1. Cell Microbiol. 2017. PMID: 28095607
We previously demonstrated that coxsackievirus B3 (CVB3) infection upregulated heat shock protein 70 (Hsp70) and promoted CVB3 multiplication. ...By using an Hsp70-overexpressing cell line infected with CVB3, we found that Hsp70 enhanced CVB3 VP1 trans …
We previously demonstrated that coxsackievirus B3 (CVB3) infection upregulated heat shock protein 70 (Hsp70) and promoted CVB3
Emodin inhibits coxsackievirus B3 replication via multiple signalling cascades leading to suppression of translation.
Zhang HM, Wang F, Qiu Y, Ye X, Hanson P, Shen H, Yang D. Zhang HM, et al. Among authors: yang d. Biochem J. 2016 Feb 15;473(4):473-85. doi: 10.1042/BJ20150419. Epub 2015 Nov 30. Biochem J. 2016. PMID: 26621875
CVB3 (coxsackievirus 3) is a primary causal agent of viral myocarditis. Emodin is a natural compound isolated from certain plant roots. In the present study, we found that emodin inhibited CVB3 replication in vitro and in mice, and now we report an unrecognized mech
CVB3 (coxsackievirus 3) is a primary causal agent of viral myocarditis. Emodin is a natural compound isolated from certain plant root
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