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palmitate oxidation is mediated by classical nuclear receptor To determine the molecular mechanism of testosterone effect on palmitate oxidation, we investigated whether this effect is mediated by classical nuclear receptor, using the specific sex hormone

on different cell types have suggested the existence of a specific membrane receptor ( Verdier-Sevrain et al . 2006 ). Rapid signaling has been shown to impact genomic activity, resulting in the integration of membrane and nuclear actions of estrogen

defect in at least one gene of the nuclear receptor superfamily ( Shih et al. 2001 ). Mutation in the short heterodimer partner (SHP) (NR0B2), which is an orphan nuclear receptor ( Seol et al. 1996 , Lee et al. 1998 , Nishizawa et al

Introduction Liver X receptor (LXR) α and β are ligand-activated transcription factors that belong to the nuclear receptor superfamily. Both LXRs are key sensors of intracellular sterol levels that trigger various adaptive mechanisms in response to

oestrogen-dependent LHRH self-priming may be a nuclear ERα action modulated by surface ERα-initiated signalling inhibition of PR action (Fig. 9 ). Table 1 List of steroid receptor ligands used indicating their action and relevant references Action

Introduction PPARγ is a nuclear receptor of the peroxisome proliferator-activated receptor family, which also includes PPARα and PPARβ/δ (for review, see Sorensen et al. 1998 , Desvergne & Wahli 1999 ). PPARγ is activated after

turn, may be influenced by other signalling pathways. Nuclear hormone receptors interact with coregulatory proteins, either coactivators, which enhance transcription, or corepressors, which repress transcription. ER contains two ‘activation functions

.1210/en.2008-1759 ) 19307418 10.1210/en.2008-1759 Levin ER Hammes SR 2016 Nuclear receptors outside the nucleus: extranuclear signalling by steroid receptors . Nature Reviews Molecular Cell Biology 17 783 – 797 . ( https://doi.org/10.1038/nrm

-kDa ligand-inducible nuclear receptor, is a member of the nuclear receptor superfamily. The effects of androgens are generally mediated by AR activation ( Chang et al . 1988 a , b , Orlic et al . 2001 ). The biological actions of androgens via

inhibitor sunitinib, which is a substrate of CYP3A4, was rapidly metabolized in patients treated with mitotane. However, the precise mechanism of CYP3A4 induction by mitotane is not well understood. The orphan nuclear receptor (NR), steroid and xenobiotic