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Abstract
Background
Results
HCV proteins induced disruption of the Golgi apparatus and co-localized with ER and mitochondria markers
HCV polyprotein expression in human HeLa and HepG2 cells induces severe morphological alterations and production of electron dense structures in the cytoplasm surrounded by membranes
Immunogold electron microscopy revealed that HCV proteins are part of the electron dense and membranous structures
HCV polyprotein expression results in mitochondrial dysfunction, as revealed by release of cytochrome c, loss of membrane potential and generation of reactive oxygen species (ROS)
Expression of HCV proteins induces apoptosis through activation of initiator and effector caspases
Identification of differentially expressed human genes in cells expressing HCV proteins
Discussion
Methods
Cells and viruses
Immunofluorescence
Electron microscopy
Embedding of infected cells in EML-812
Embedding of infected cells in Lowicryl K4M
Immunogold labeling of ultrathin sections
Imaging and measurements
Quantification of mitochondrial membrane potential (DYm) and production of reactive oxygen species (ROS)