PKR (Protein kinase-R) is a ubiquitously expressed serine-threonine kinase that has been implicated as a signal integrator in translational and transcriptional control pathways. PKR mediates apoptosis induced by many different stimuli, such as LPS (Lipopolysaccharides), IFN-Gamma (Interferon-Gamma), cytokines, growth factor, viral infection, or serum starvation. PKR activity is regulated by external signals, which act on proteins, which interact with PKR. Among the proteins identified so far are p58, a cellular protein, K3L, the product of a gene of vaccinia virus, PACT (Protein Activator Of Interferon-Induced Protein Kinase) and p67, an interferon-induced glycoprotein (Ref.1). Human PKR is 68 kDa with a 20 kDa N-terminal dsRBD (dsRNA-Binding Domain) and a C-terminal protein kinase domain. The dsRBD is composed of two copies of the dsRNA-binding motif (dsRBM I and dsRBM II), [...]