RNA-dependent protein kinase, also known as PKR (protein kinase R), is an enzyme that plays a crucial role in the cellular response to viral infection. As the name suggests, it is a protein kinase that is activated by specific RNA molecules.
When a cell is infected by a virus, viral RNA is produced and released into the cytoplasm. PKR recognizes double-stranded RNA, a characteristic feature of viral RNA, and becomes activated. Once activated, PKR phosphorylates (adds a phosphate group to) a number of target proteins, leading to the inhibition of protein synthesis within the infected cell. This mechanism helps to restrict viral replication and prevent the spread of infection to neighboring cells.
The activation of PKR initiates a cascade of events that trigger an antiviral immune response in the cell. Phosphorylation of PKR leads to its dimerization, enabling it to phosphorylate eukaryotic initiation factor 2 alpha (eIF2α), a key protein involved in mRNA translation. This results in the shutdown of global protein synthesis, while allowing the translation of specific antiviral proteins necessary for viral defense.
Increased activity of PKR has been observed in a variety of viral infections and is implicated in the pathogenesis of several diseases, including viral hepatitis, influenza, and viral encephalitis. Understanding the role of PKR in these infections provides potential targets for therapeutic interventions and the development of antiviral drugs.
In summary, RNA-dependent protein kinase is an important cellular enzyme that plays a central role in the antiviral response. Its activation efficiently curtails protein synthesis within infected cells, restricts viral replication, and helps to mount an immune response against invading viruses.
