The RGD motifs within the C-terminus of coxsackie virus A9 and human parechovirus 1 VP1 proteins were fused to the N-terminus of the major envelope glycoprotein, gp64, of Autographa californica multiple nucleopolyhedrovirus.
The RGD motifs within the C-terminus of coxsackie virus A9 and human parechovirus 1 VP1 proteins were fused to the N-terminus of the major envelope glycoprotein, gp64, of Autographa californica multiple nucleopolyhedrovirus.
The RGD motifs within the C-terminus of coxsackie virus A9 and human parechovirus 1 VP1 proteins were fused to the N-terminus of the major envelope glycoprotein, gp64, of Autographa californica multiple nucleopolyhedrovirus.
Therefore, mortality, cardiac inflammation, and function were assessed in TSP-2-null (KO) and wild-type (WT) mice in human Coxsackie virus B3 (CVB3)-induced myocarditis.
Three groups of mice were established: 5 mice in a control group injected with saline, 15 in the model group injected with coxsackie virus B<sub>3</sub> (CVB) and 15 in the intervention group injected with CVB<sub>3</sub> but treated with the p38 MAPK inhibitor SB203580.
Three groups of mice were established: 5 mice in a control group injected with saline, 15 in the model group injected with coxsackie virus B<sub>3</sub> (CVB) and 15 in the intervention group injected with CVB<sub>3</sub> but treated with the p38 MAPK inhibitor SB203580.
Three groups of mice were established: 5 mice in a control group injected with saline, 15 in the model group injected with coxsackie virus B<sub>3</sub> (CVB) and 15 in the intervention group injected with CVB<sub>3</sub> but treated with the p38 MAPK inhibitor SB203580.
Three groups of mice were established: 5 mice in a control group injected with saline, 15 in the model group injected with coxsackie virus B<sub>3</sub> (CVB) and 15 in the intervention group injected with CVB<sub>3</sub> but treated with the p38 MAPK inhibitor SB203580.
Three groups of mice were established: 5 mice in a control group injected with saline, 15 in the model group injected with coxsackie virus B<sub>3</sub> (CVB) and 15 in the intervention group injected with CVB<sub>3</sub> but treated with the p38 MAPK inhibitor SB203580.
Three groups of mice were established: 5 mice in a control group injected with saline, 15 in the model group injected with coxsackie virus B<sub>3</sub> (CVB) and 15 in the intervention group injected with CVB<sub>3</sub> but treated with the p38 MAPK inhibitor SB203580.
Three groups of mice were established: 5 mice in a control group injected with saline, 15 in the model group injected with coxsackie virus B<sub>3</sub> (CVB) and 15 in the intervention group injected with CVB<sub>3</sub> but treated with the p38 MAPK inhibitor SB203580.
Three groups of mice were established: 5 mice in a control group injected with saline, 15 in the model group injected with coxsackie virus B<sub>3</sub> (CVB) and 15 in the intervention group injected with CVB<sub>3</sub> but treated with the p38 MAPK inhibitor SB203580.
We have previously shown that coxsackievirus infection facilitates the ubiquitin/proteasome processing of the cell-cycle protein cyclin D1 and the tumor suppressor p53, which raises the possibility that the ubiquitin/proteasome pathway may be used by virus to promote viral replication.
We have recently demonstrated that SQSTM1 is cleaved after coxsackievirus infection, resulting in the disruption of SQSTM1 function in selective autophagy.NBR1 is a functional homolog of SQSTM1.