Role of JAK-STAT Pathway in Antiviral Defense: Activation by Type I IFNs in Infected Cells

The proteins made by infected cells after type I IFNs bind to the cell activates the ____________-___________

The proteins made by infected cells after type I interferons (IFNs) bind to the cell activates the JAK-STAT pathway

The proteins made by infected cells after type I interferons (IFNs) bind to the cell activates the JAK-STAT pathway.

The JAK-STAT pathway is a critical signaling cascade that is activated in response to the binding of type I IFNs to their specific receptors on the surface of infected cells. This pathway plays a key role in the innate immune response against viral infections.

When type I IFNs bind to their receptors, it triggers the activation of Janus kinases (JAKs), a family of enzymes associated with the receptor complex. The activated JAKs, in turn, phosphorylate the signal transducers and activators of transcription (STAT) proteins.

The phosphorylated STAT proteins form dimers and translocate into the nucleus where they act as transcription factors. By binding to specific DNA sequences known as interferon-stimulated response elements (ISREs), these STAT dimers regulate the expression of a variety of genes involved in antiviral defense.

This includes the production of important antiviral effector molecules, such as protein kinase R (PKR), 2′-5′-oligoadenylate synthase (OAS), and Mx proteins, which are responsible for inhibiting viral replication within infected cells.

Additionally, the JAK-STAT pathway also induces the production of various cytokines and chemokines, which contribute to the recruitment and activation of other components of the immune system.

Overall, the activation of the JAK-STAT pathway by type I IFNs is a crucial step in the cellular antiviral response, leading to the production of effector molecules that help to limit viral replication and spread, and ultimately aid in the clearance of the infection.

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