state of survival plasma core requirements

We address how RIPK1 mutations or aberrant regulation is associated with inflammatory and autoimmune disorders and cancer. In this Review, we discuss the molecular mechanisms that regulate RIPK1 to maintain homeostasis and cellular survival in healthy cells, yet drive cell death in a context-dependent manner. Its tight regulation involves multiple layers of post-translational modifications. Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) is emerging as a critical stress sentinel that functions as a molecular switch, governing cellular survival, inflammatory responses and immunogenic cell death signalling.

It facilitates the exchange of information between the dying cell and cells of the tissue microenvironment, particularly immune cells, alerting and recruiting them to the site of disturbance. Recent advancements in our understanding of the intricate signals originating from dying cells have revealed that cell death serves as more than just an end point. Cell death and inflammation are closely linked arms of the innate immune response to combat infection and tissue malfunction.

State of survival plasma core requirements