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Both GRα and PPARα can inhibit NF-κB mediated inflammatory gene expression by transrepressing NF-κB.
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These studies suggest that growth factor RTKs may play a pivotal role in mediating inflammatory genes regulation through ROS signal in several diseases including the CNS disorders.
The ERα was functional in these cells, because WAY-169916 could effectively block the TNF-α-mediated inflammatory gene expression of IL-6, TNF-α, and ICAM-1.
In particular, resistance to GC-mediated inflammatory gene repression, possibly resulting from diminished availability of corepressors or elevated expression of the dominant negative isoform, GRβ, is implicated in major inflammatory diseases such as severe asthma and chronic obstructive pulmonary disease (2, 3, 104, 107, 108).
A body of evidence is developing that identifies a possible link between the two modes of actions via "receptor-interacting-protein-of-140-kDa" (RIP140), a co-repressor of PPARγ as well as a co-activator of NFκB-mediated inflammatory gene expression.
The proinflammatory function of NF-κB in renal cells is also subject to regulation by the p50/p50 homodimer, a κB-specific repressor that is induced during experimental renal injury and serves as a feedback repressor of NF-κB-mediated inflammatory gene induction [ 90, 91].
Therefore, kallistatin protects against sepsis-induced inflammation, organ damage and mortality by antagonizing TNF-α and HMGB1-mediated inflammatory gene expression, and by inducing SOCS3 synthesis.
Finally, WAY-169916 was effective in suppressing tumor necrosis factor-α-mediated inflammatory gene expression in fibroblast-like synoviocytes isolated from patients with RA.
Although studies of the role of mel in the anti-tumoral suppression of TLR4/NFkB are scarce, in vitro data showed that mel promotes the inhibition of TLR4-mediated inflammatory genes via MyD88-dependent signaling pathway [ 32], and that mel acts as a TLR4/MyD88 antagonist [ 33].
Several genes mediating inflammatory processes were also highly up-regulated, such as the chemokine receptor CCR5, and the glycoprotein CD74.
These studies found a potential role for AR in mediating inflammatory responses during PCa progression since gene signatures of wound healing responses are very similar to genes identified in studies of progressive breast cancer with high metastatic potential (Chang et al, 2005).
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