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We found PDGF induced Rad expression in a dose- and time-dependent manner, which Egr-1 and its partners mediated this induction.
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Several transacting proteins mediating this induction have been identified, including both activators (xylanase regulator 1 (XYR1), activator of cellulase expression 2 (ACE2), heme activation protein (HAP2/3/5) complex) as well as repressors (ACE1 and the carbon catabolite repressor protein 1 (CRE1)) [ 7- 10].
One of the molecules mediating this gene induction is a regulatory protein called nuclear factor-κB, which activates many innate immune genes.
Pathways potentially mediating this association include induction of systemic inflammation [ 3, 4] and oxidative stress [ 5, 6], as well as changes in ion channel function in myocardial cells [ 7] or cardiac autonomic function [ 8– 10].
In this case, Egr1 mediates the induction of p35 activating Cdk5, which is necessary for neurite-like outgrowth.
These findings indicate that GH(4 C(1) cells express purinogenic receptors with selectivity consistent with the P2X7 subtype and that this receptor pathway mediates the induction of the c-fos luciferase reporter gene by ATP and the putative Pfiesteria toxin.
In one case, this is mediated by induction of a transcriptional mediator, mdt-15, and is required in part for the beneficial effects of the intestinal activation of DAF-16 by daf-2 on whole-organism aging (Zhang et al., 2013).
AA is shown to mediate the induction of some low pH and oxidative stress response genes.
Also, 4-HNE is reported to mediate the induction of neuronal apoptosis in the presence of oxidative stress [18].
In the latter scenario, homeobox transcription factors may mediate the induction of factors involved in adipose tissue remodeling.
It has been previously proposed that FGFR4 mediates the induction of hepatocyte proliferation by FGF19 [16] (French, D.M., in preparation).
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