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  • VP2 of Infectious Bursal Disease Virus Induces Apoptosis via Triggering Oral Cancer Overexpressed 1 (ORAOV1) Protein Degradation.

VP2 of Infectious Bursal Disease Virus Induces Apoptosis via Triggering Oral Cancer Overexpressed 1 (ORAOV1) Protein Degradation.

Frontiers in microbiology (2017-08-05)
Yao Qin, Zhichao Xu, Yongqiang Wang, Xiaoqi Li, Hong Cao, Shijun J Zheng
ZUSAMMENFASSUNG

Infectious bursal disease (IBD) is an acute, highly contagious and immunosuppressive avian disease caused by IBD virus (IBDV). Cell apoptosis triggered by IBDV contributes to the dysfunction of immune system in host. VP2 of IBDV is known to induce cell death but the underlying mechanism remains unclear. Here we demonstrate that VP2 interacts with the oral cancer overexpressed 1 (ORAOV1), a potential oncoprotein. Infection by IBDV or ectopic expression of VP2 causes a reduction of cellular ORAOV1 and induction of apoptosis, so does knockdown of ORAOV1. In contrast, over-expression of ORAOV1 leads to the inhibition of VP2- or IBDV-induced apoptosis, accompanied with the decreased viral release (

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Sigma-Aldrich
Monoklonaler ANTI-FLAG® M2-Antikörper in Maus hergestellte Antikörper, 1 mg/mL, clone M2, affinity isolated antibody, buffered aqueous solution (50% glycerol, 10 mM sodium phosphate, and 150 mM NaCl, pH 7.4)
Sigma-Aldrich
Adenosin-5′-diphosphoribose Natriumsalz, ≥93%
Sigma-Aldrich
Anti-ORAV1 antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
MISSION® esiRNA, targeting human ORAOV1