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Results reveal that the retinoid receptors interaction with circulating hormonal signals MOP4 and CLOCK causes retinoic acid phase shifts in Per2 mRNA and in the smooth muscle cells, leading to a nuclear receptor-mediated hormonal signaling for regulating a peripheral clock in the vasculature.

Recently published work that establishes a specific role for the nuclear receptor FXR in cholesterol catabolism pathways and in repression of the CYP7A1 gene and regulation by nuclear receptors, is discussed in this review article. The rate-limiting step of the neutral bile biosynthesis pathway is catalyzed by the cytochrome P450 cholesterol 7alpha-hydroxylase or CYP7A1. Lipid homeostasis in vertebrates, that is, the acquisition, synthesis and metabolism of cholesterol, is important. As mediators of organ physiology, nuclear hormone receptors, and other proteins are thought to play a vital role in the processes by controlling the transcription of genes encoding the transporters, the apoplipoproteins, as well as catabolic and synthetic enzymes. Implications for future drug development in treatment of hypercholesterolemia and cholestasis are important.

Findings of a recent study of metazoan development suggest that specific combinations of histone deacetylases and corepressors mediate the gene-specific actions of DNA-bound repressors in multiple organ system development. It was found, surprisingly, that N-coR and a specific deacetylase were required for transcriptional activation of one class of retinoic acid response element.

The authors dicuss the role of the nuclear bile acid receptor FXR/BAR as an intracellular bile acide sensor in lipid and bile accid homeostasis.

Several studies revealed the potential physiological roles of three nuclear orphan receptors, namely, LXRL, CPF (NR5A2) and FXR (NR1H4). These receptors were found to be involved in the body's controlled elimination of excess cholesterol and regulation of the catabolic process by preventing the conversion of cholesterol into bile acids. The nuclear orphan receptors' physiological function as a regulator of cholesterol accumulation is one of the body's defense against heart attacks.

Glucocorticoid receptors (GR) are genetic regulators able to modulate transcription either through direct DNA interaction or transrepression of other regulatory elements. The relative contributions of DNA interaction and transrepression on the gene regulation function of GR are investigated in mice unable to dimerize receptors which is a necessary step before the receptor can interact with DNA. Results reveal that DNA binding is not essential to genetic regulation by GR.

Endocrine disruptors, a group of environmental agents that mimic or interfere with the functions of endogenous hormones, are raising global concerns due to their potential adverse health effects on humans and animals. Experts were discussing the possibility of using the receptor theory for the development of public policy for risk assessment and prevention. Endocrine disruptors are widely perceived to have the ability to interact with receptors as agonists, antagonists, partial agonists or negative antagonists.

SMRT, Sin3, and N-CoR establish protein-to-protein link between deacetylases and DNA-bound repressors hence, the term corepressors. These corepressors interact with each other and influence nuclear receptor to remodel chromatin structure without altering the regulatory complex through the help of hormone dependent adaptor HDAC. Transcriptional repression is achieved through regulation of chromatin structure resulting in an opposed cellular differentiation.

The activation of G protein alpha subunit, a(s), by hormone receptor or a GTPase-inhibiting mutation results in activation-induced depalmitoylation and increased rate of attachment of the a(s) pool by (3H) palmitate. Regulation of palmitoylation is a feature of a number of proteins. Palmitoylation cycles control membrane activity and subcellular location.

Results demonstrate that the Drosophila transforming growth factor(TGF)-beta/activin signaling pathway is partially involved in neuronal remodeling by regulating the ecdysone receptor, EcR-B1, expression. Data indicate that knocking out dActivin inhibits EcR-B1 expression in the late third instar larval brain. Furthermore, the TGF-beta/activin signaling mediates remodeling of mushroom body neurons through regulating EcR-B1 expression.