GCs act via the GR and after binding of GC this ligand-bound complex translocates into the nucleus where it can either bind to GC responsive elements or directly to transcription factors.
Accordingly, the AR-V7 and AR-V567es have been shown to translocate into the nucleus, bind to AR responsive elements, and activate/suppress gene transcription in vitro without the need for ligand binding [14], [16], [17].
In the classical mechanism, ERs directly bind to estrogen responsive elements (EREs) located in the promoter region of target genes.
Classically, NRs are ligand-activated transcription factors which bind to specific responsive elements located in the promoter regions of their target genes and recruit transcriptional coactivators.
LXRs, when ligand-activated by oxysterols, heterodimerize with the retinoid X receptor (RXR) and bind to LXR responsive elements on the DNA [ 27], where they induce the transcription of lipogenic genes such as SREBP-1C, FAS, ABCA1, and ACC1.
Besides binding to GCC box, these transcription factors also bind to dehydration responsive element (DRE /C-repeat (CRT) involveDRE /C-repeat salt and CRTd stress responses [ 60].
Under hypoxic conditions, HIF-1 is transactivated and translocated to the nuclei where it binds to hypoxic responsive elements (HRE) and upregulates a series of genes essential for adaptation of the tissues to hypoxia (7).
Once there, the GR forms into a homodimer, binds to glucocorticoid responsive elements (GRE) within genomic DNA, leading to an increase (trans-activation) in the expression of anti-inflammatory genes or, less commonly, repression of inflammatory genes (cis-repression).
Several studies have focused on the transcriptional regulation of TNF-α looking at transcription factors that bind to the responsive element sites within the TNF-α promoter.
