Skip to Content
Merck
  • 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
ABSTRACT

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 (

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Monoclonal ANTI-FLAG® M2 antibody produced in mouse, 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
MISSION® esiRNA, targeting human ORAOV1
Sigma-Aldrich
Anti-ORAV1 antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Adenosine 5′-diphosphoribose sodium salt, ≥93%