Finally, immunohistochemical analysis of subunit expression revealed distinct intracellular localization of the 26S proteasomal subunits at baseline and confirmed upregulation of distinct subunits following NO exposure. In conclusion, NO reversibly inhibits the catalytic activity of the 26S proteasome through S-nitrosylation and differentially regulates proteasomal subunit expression. This

may be one mechanism by which NO exerts its effects on the cell cycle and inhibits cellular proliferation in the vasculature. Published by Elsevier Inc.”
“Increasing evidence points to the importance of the interferon (IFN) response in determining the host range and virulence of African swine fever Selleck Tariquidar virus (ASFV). Infection with attenuated strains of ASFV leads to the upregulation of genes controlled by IFN pathways, including myxovirus resistance (Mx) genes that are potent effectors of the antiviral state. Mx gene products are known to inhibit the replication of many negative-sense single-stranded RNA viruses, as well as double-stranded RNA viruses, positive-sense single-stranded RNA viruses, and the reverse-transcribing DNA virus hepatitis B virus. Here, we provide data that extend the known range of viruses inhibited by Mx to include the large double-stranded DNA viruses. Stably transfected Vero cells expressing human MxA protein

did not support ASFV plaque formation, and virus replication in these cells was reduced 100-fold compared with that in control cells. In contrast, ASFV replication in cells Selleck Cyclosporin A expressing MxB protein or a mutant MxA protein was similar to that in control Vero cells. There was a drastic reduction in ASFV late protein synthesis in MxA-expressing

cells, correlating with the results of previous work on the effect of IFN on viral replication. Strikingly, the inhibition of ASFV replication was linked to the recruitment of MxA FK506 solubility dmso protein to perinuclear viral assembly sites, where the protein surrounded the virus factories. Interactions between ASFV and MxA were similar to those seen between MxA and different RNA viruses, suggesting a common inhibitory mechanism.”
“Nitric oxide (NO) is a bioactive gaseous, multifunctional molecule playing a central role and mediating a variety of physiological processes and responses to biotic and abiotic stresses including heavy metals. The present study investigated whether NO applied exogenously as sodium nitroprusside (SNP) has any protective role against arsenic (As) toxicity in Oryza sativa (rice). Treatment with 50 mu M SNP (a NO donor) significantly ameliorated the As-induced (25 or 50 mu M) decrease in root and coleoptile length of rice. Further, As-induced oxidative stress measured in terms of malondialdehyde (MDA), superoxide ion (O(2)(-center dot)), root oxidizability and H(2)O(2) content was lesser upon supplementation of NO. It indicated a reactive oxygen species (ROS) scavenging activity of NO.