Expression of ORFV002 in cells, while not affecting phosphorylation or nuclear translocation of NF-kappa B-p65, markedly decreased TNF-alpha- and wild-type-virus-induced acetylation of NF-kappa B-p65, a p300-mediated nuclear modification of NF-kappa B-p65 that regulates its transactivating activity. ORFV002 was shown to colocalize and interact with NF-kappa B-p65, and expression of ORFV002 in cell cultures resulted in a reduced interaction of NF-kappa B-p65 with p300, suggesting that ORFV002 interferes with NF-kappa B-p65/p300 association. Deletion of ORFV002 from the OV-IA82 genome had no significant effect on ORFV pathogenesis in sheep, indicating that ORFV002

is nonessential for virus virulence in the natural

host. selleck This represents the first description of a nuclear inhibitor of NF-kappa B encoded by a poxvirus.”
“Accumulating evidence demonstrates astrocytic crucial click here roles in the brain, but the molecular basis underlying astrocytic intracellular protein trafficking remains to be elucidated. The present study reports the identification of novel protein, brain-derived integrating factor-1 (BDIF1), which comprises TBC (Tre-2/Bub2/Cdc16), SH3, RUN domains. The amino acid sequence putatively coding TBC domain in BDIF1 implied its potential to interact with small GTP-binding proteins (G-proteins), and further analyses by co-immunprecipitation and immunocytochemical staining demonstrated that BDIF1 bound to astrocytic gap junctional protein, connexin-43 (Cx43). Our present data shows that BDIF1 potentially functions in molecular trafficking in astrocytes. (C) 2011 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Viruses cause about 15% of the cancers that are still the leading causes of human mortality. The discovery of viral oncogenes has

enhanced our understanding of viral oncogenesis. However, the underlying molecular mechanisms of virus-induced cancers are complex and require further investigation. The present study has attempted to investigate the effects of the microRNAs (miRNAs) about encoded by Marek’s disease virus 1 (MDV1), a chicken herpesvirus causing acute T-cell lymphomas and solid visceral tumors in chickens, on anti-cancer drug-induced apoptosis and identify the targets of the miRNAs. The results showed that of the total 14 miRNAs encoded by MDV1, MDV1-miR-M3 significantly promoted cell survival under treatment with cisplatin, a widely used chemotherapy drug. MDV1-miR-M3 suppressed cisplatin-induced apoptosis by directly downregulating expression at the protein but not the mRNA level of Smad2, a critical component in the transforming growth factor beta signal pathway. Our data suggest that latent/oncogenic viruses may encode miRNAs to directly target cellular factors involved in antiviral processes including apoptosis, thus proactively creating a cellular environment beneficial to viral latency and oncogenesis.