Sentence examples for many proinflammatory genes from inspiring English sources

ZFP36 destabilizes the mRNA of many proinflammatory genes by binding to an AU-rich element (ARE) located at the 3' untranslated region (UTR) of their mRNA [11], [12].

The expression of many proinflammatory genes is enhanced by the transcription factor nuclear factor kappa beta (NF-κB).

In addition, it activates nuclear factor-κB (NF-κB), a central transcriptional activator of many proinflammatory genes [ 18, 26, 28].

Inflammation is a complex process involving a network of cytokines responsible for the expression of many proinflammatory genes.

Interestingly, the activities of NFκB and NFAT together are responsible for the transcription of many proinflammatory genes, including several genes coding for cytokines and chemokines [ 29, 30].

Since NF- κB controls expression of many proinflammatory genes, IRE1 is therefore suggested to provide a link between the ER stress and inflammation [ 33].

EPA can also affect the activity of the proinflammatory transcription nuclear factor κB (NF-κB), which regulates the expression of many proinflammatory gene-encoding adhesion molecules, cytokines, chemokines and other effectors of the innate immune response system [ 10].

Previous studies showed that expression of many proinflammatory cytokine genes, including IFN- α, IFN- γ, iNOS, IL-1 β, IL-6 and IL-18, have been enhanced in chicken following infection with MDV [ 22– 25].

IFN β is released from infected cells, binds to the IFN α/ β receptor (IFNAR1 and IFNAR2) on neighboring cells, and induces a diverse ISG set that includes many antiviral and proinflammatory genes.

Activation of NF-κB serves to induce the expression of multiple proinflammatory genes, many of which are also regulated by HIF-1α [ 78, 111].

The canonical pathway mainly activates the transcription of many proinflammatory cytokine and chemokine genes that initiate and propagate innate immune responses [ 8].