Your browser doesn't support javascript.
loading
Equine arteritis virus induced cell death is associated with activation of the intrinsic apoptotic signalling pathway.
Cholleti, Harindranath; Paidikondala, Maruthibabu; Munir, Muhammad; Hakhverdyan, Mikhayil; Baule, Claudia.
  • Cholleti H; R&D Unit for Virology, Department of Virology, Immunobiology and Parasitology of the National Veterinary Institute (SVA), Ulls väg 2B, SE-751 89 Uppsala, Sweden.
Virus Res ; 171(1): 222-6, 2013 Jan.
Article en En | MEDLINE | ID: mdl-23079113
ABSTRACT
Equine arteritis virus (EAV) causes a respiratory and reproductive disease in horses, equine viral arteritis. Though cell death in infection with EAV is considered to occur by apoptosis, the underlying molecular mechanism has not been extensively elucidated. We investigated the expression of mRNA of pro-apoptotic and caspase genes during EAV infection in BHK21 cells, a well-established cell type for EAV replication. Using a SYBR Green real-time PCR, mRNA of p53, Bax, caspase 3 and caspase 9 were found up-regulated in a time dependent manner in EAV infected cells. Western blot analysis for caspase 3 and caspase 9 showed expression of cleaved forms of these proteins during EAV infection. In addition, a luminescence-based cell assay for caspase 3/7 activation as a hallmark in apoptosis confirmed apoptotic cell death. The findings demonstrate that cell death in EAV infected BHK21 cells results from apoptosis mediated through the intrinsic signalling pathway.
Asunto(s)

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Transducción de Señal / Apoptosis / Infecciones por Arterivirus / Equartevirus / Enfermedades de los Caballos Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Año: 2013 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Transducción de Señal / Apoptosis / Infecciones por Arterivirus / Equartevirus / Enfermedades de los Caballos Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Año: 2013 Tipo del documento: Article