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NADPH oxidases (Nox enzymes) are critical mediators of both physiologic and pathophysiologic processes.
They are mediators of both adaptive and innate immune regulation supporting the theory that a close interplay of adaptive and innate immune regulation is critical in asthma.
These multimeric enzymes are mediators of both intra- and extracellular vectorial proton transport in all eukaryotic cells.
Cytokines are ultimate mediators of both responses.
Segmental duplications have been recognized as important mediators of both gene and genome evolution [ 1- 9].
C1q and the classical complement pathway are critical mediators of both ASH and NAFLD.
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Collectively, our data highlights IFNγ, IL-22 and IL-17 family as critical mediators of host immunity both in the acute and in the effector phase of C. jejuni infection.
An important mediator of both tumorigenesis and resistance to treatment involves inhibition of apoptosis [7].
Fractalkine (CX3CL1) is a potential mediator of both atherosclerosis and metabolic disease.
Recently, we identified granulocyte-macrophage colony-stimulating factor (GM-CSF) as a critical mediator of both tumor necrosis factor-α– (TNF; modeling inflammation) and thrombin-induced (modeling abruption) weakening of the fetal membranes.
Therefore, a model has evolved whereby TIEG1 serves as an important mediator of both Runx2 expression levels and Runx2 transcriptional activity in osteoblasts (Figure 10).
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