At the most basic level, ligand-bound NHRs can directly bind to response elements in gene promoters and recruit co-activators or co-repressors to alter the activity of the transcriptional machinery [ 43].
In the case of PPARβ/δ [25], as with other PPARs, the genomic pathway is thought to involve binding to retinoid X receptor (RXR) and the formation of heterodimers which then bind to response elements of target genes.
Intracellular PKAcα levels and phosphorylation of HSF1 at S320 were both required for HSF1 to be localized to the nucleus, bind to response elements in the promoter of an HSF1 target gene (hsp70.1) and activate hsp70.1 after stress.
Using the affinity-based in vitro genomic selection procedure, we have shown for the first time that Ac-DAF-16 directly binds to response elements in the hookworm genome.
These ligand-depended transcription factors bind to response elements (RAREs or RXREs) in the promoter region of modulated genes [ 4].
When Hsp90 is functional and can assist in proper folding of GR, addition of the hormone deoxycorticosterone leads to activation of GR such that it can dimerize, translocate to the nucleus, and bind to response elements.
Upon ligand binding, PPARs form heterodimers with the retinoid X receptor (RXR), another nuclear receptor, and bind to response elements located in the promoter region of their target genes [8].
The induction of P450 4A enzymes by peroxisome proliferators (PPs) and fatty acids is mediated by the peroxisome proliferator activated receptor α (PPARα) that binds to response elements in target genes as a heterodimer with the retinoid X receptor (RXR).
The tumor suppressor p53, a nuclear transcription factor, binds to response elements in the promoter region of many genes and plays a pivotal role in apoptosis.
