RA binding to RAR/RXR heterodimers bound to a regulatory DNA element leads to a cascade of events resulting in recruitment of transcriptional co-activators and initiation of transcription [35], [37].
In contrast to its interaction with the RIBS element, where it acts solely as an activator, the binding of GABP alpha/beta to the UP element appears to also have a repressor function as mutation of the GABP alpha/beta recognition element leads to loss of UP mediated repression.
Translocation of HIF-1 to the nucleus and binding to hypoxic response elements leads to the transcription and translation of numerous genes (Semenza et al, 1994; Carmeliet et al, 1998; Pugh and Ratcliffe, 2003).
NRF2 recognizes the cis-acting antioxidant response element (ARE) in target gene promoters and, upon binding, typically leads to increased expression of these genes.
(vii) Phosphorylation of cAMP response element-binding protein (CREB) leads to the transcription of PER1, which contributes to the shifting of the circadian phase.
Ligand binding leads to PR activation, dimerization, and binding of dimers to promoters at progesterone responsive elements (PREs), followed by interaction with coregulators and altered transcription [ 27].
Therefore mutations can convert an Alu element into a dominant exon when completely removing hnRNP C binding, which can lead to disease.
IFN-γ/receptor binding leads to subsequent endocytosis and IFN-γ nuclear localization sequence (NLS -guided biNLS -guidede IFN-γ-activated sequence (GAS) response element in the promoter region of IFN-γ-activated genes, such as IDO.
Next, we compared these motifs with all known sequence-specific recognition elements of transcription factors, which led to the identification of several binding motifs of well-known adipogenic transcription factors including PPARγ and C/EBPγ (Ge et al., 2008).
