Recombinant plasmid pcDNA3.1-NS1 containing the complete NS1 gene of parvovirus H-1 was constructed and characterized by restriction enzyme digestion and sequence analysis.
Recombinant plasmid pcDNA3.1-NS1 containing the complete NS1 gene of parvovirus H-1 was constructed and characterized by restriction enzyme digestion and sequence analysis.
As shown previously, a parvovirus genome containing a deleted NS1 gene was excised from a bacterial plasmid and replicated when a wild-type NS1 gene was provided in trans but failed to be excised and replicate when the mutant NS1 gene was supplied.
As shown previously, a parvovirus genome containing a deleted NS1 gene was excised from a bacterial plasmid and replicated when a wild-type NS1 gene was provided in trans but failed to be excised and replicate when the mutant NS1 gene was supplied.
In summary, these findings indicate that PPV could induce SLCs apoptosis and a decrease of progesterone production in vivo and in vitro via p38 MAPK signaling and p53-dependent mitochondrial pathway, which provides the potential clinical therapy methods for PPV infection.
In summary, these findings indicate that PPV could induce SLCs apoptosis and a decrease of progesterone production in vivo and in vitro via p38 MAPK signaling and p53-dependent mitochondrial pathway, which provides the potential clinical therapy methods for PPV infection.
In summary, these findings indicate that PPV could induce SLCs apoptosis and a decrease of progesterone production in vivo and in vitro via p38 MAPK signaling and p53-dependent mitochondrial pathway, which provides the potential clinical therapy methods for PPV infection.
In summary, these findings indicate that PPV could induce SLCs apoptosis and a decrease of progesterone production in vivo and in vitro via p38 MAPK signaling and p53-dependent mitochondrial pathway, which provides the potential clinical therapy methods for PPV infection.
In summary, these findings indicate that PPV could induce SLCs apoptosis and a decrease of progesterone production in vivo and in vitro via p38 MAPK signaling and p53-dependent mitochondrial pathway, which provides the potential clinical therapy methods for PPV infection.
In summary, these findings indicate that PPV could induce SLCs apoptosis and a decrease of progesterone production in vivo and in vitro via p38 MAPK signaling and p53-dependent mitochondrial pathway, which provides the potential clinical therapy methods for PPV infection.
In summary, these findings indicate that PPV could induce SLCs apoptosis and a decrease of progesterone production in vivo and in vitro via p38 MAPK signaling and p53-dependent mitochondrial pathway, which provides the potential clinical therapy methods for PPV infection.
In summary, these findings indicate that PPV could induce SLCs apoptosis and a decrease of progesterone production in vivo and in vitro via p38 MAPK signaling and p53-dependent mitochondrial pathway, which provides the potential clinical therapy methods for PPV infection.
Infection with a recombinant parvovirus vector carrying the luciferase gene under control of parvovirus promoter P38 led to higher transgene activities in hepatoma cells than in the hepatocytes.
Infection with a recombinant parvovirus vector carrying the luciferase gene under control of parvovirus promoter P38 led to higher transgene activities in hepatoma cells than in the hepatocytes.
Infection with a recombinant parvovirus vector carrying the luciferase gene under control of parvovirus promoter P38 led to higher transgene activities in hepatoma cells than in the hepatocytes.