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recruitment of specific sets of coregulators. To follow-up on this hypothesis, in the present study, we aimed to identify possible ligand-specific recruitment of coregulators to TRB1 isoforms. Here, we identified Jab1 as a TRB1 partner and showed that this
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the receptor to interact with the transcriptional machinery assembled on the promoter and thus, by analogy with other transcription factors, there must exist coregulators that bridge the activation function in the NR to the promoter complex. The
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by binding the ligand to form a complex that, upon homodimerization, interacts with various co-regulators to target E-responsive gene promoters, leading to transcriptional activation, and the synthesis of gene products that modify cellular phenotype
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and repressing co-regulators ( Heldring et al . 2007 ). Recent genome-wide binding site mapping studies have shown that the majority of ER-binding sites are situated far away from the promoters that they affect ( Carroll et al . 2005 , 2006 , Lin
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
Corcept Therapeutics, Menlo Park, CA, USA
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
Corcept Therapeutics, Menlo Park, CA, USA
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reference genes (RG) Hprt , GusB and Gapdh , as previously described ( Blažević et al. 2022 ). Microarray assay for real-time coregulator-nuclear receptor interaction GR-coregulator interactions were assessed in the presence of 1 µM cortisol
Department of Biochemistry, Faculty of Medicine, University of Hong Kong, Pokfulam, Hong Kong SAR, China
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Department of Biochemistry, Faculty of Medicine, University of Hong Kong, Pokfulam, Hong Kong SAR, China
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Department of Biochemistry, Faculty of Medicine, University of Hong Kong, Pokfulam, Hong Kong SAR, China
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Department of Biochemistry, Faculty of Medicine, University of Hong Kong, Pokfulam, Hong Kong SAR, China
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Department of Biochemistry, Faculty of Medicine, University of Hong Kong, Pokfulam, Hong Kong SAR, China
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Introduction Transcriptional coregulators provide important regulatory flexibility in the cellular responsiveness to hormones and extracellular signals. The physiologic importance of coregulator function is highlighted by the
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Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
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complicated by, and dependent on, the binding of coregulators (coactivators or corepressors) to the receptor–ligand complex. Coregulators are recruited to specific domains of the ER protein named activating functions (AF)-1 and 2, subsequently enabling or
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targets of FGF21 (PGC1α and SIRT1) and reported activators of PDK4 expression were measured ( Wende et al . 2005 ). At the end of the infusion period there was a significant increase in protein abundance of the key hepatic transcriptional co-regulators of
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Over the 70 or so years since their discovery, there has been continuous interest and activity in the field of corticosteroid functions. However, despite major advances in the characterisation of receptors and coregulators, in some ways we still lack clear insight into the mechanism of receptor activation, and, in particular, the relationship between steroid hormone structure and function remains obscure. Thus, why should deoxycorticosterone (DOC) reportedly be a weak mineralocorticoid, while the addition of an 11β-hydroxyl group produces glucocorticoid activity, yet further hydroxylation at C18 leads to the most potent mineralocorticoid, aldosterone? This review aims to show that the field has been confused by the misreading of the earlier literature and that DOC, far from being relatively inactive, in fact has a wide range of activities not shared by the other corticoids. In contrast to the accepted view, the presence of an 11β-hydroxyl group yields, in corticosterone or cortisol, hormones with more limited functions, and also more readily regulated, by 11β-hydroxysteroid dehydrogenase. This interpretation leads to a more systematic understanding of structure–function relationships in the corticosteroids and may assist more rational drug design.
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Among all the androgens that stimulate or control the development and maintenance of body composition, testosterone could be the most well known and important due to its linkage to many diseases, including the metabolic syndrome, type 2 diabetes, and cardiovascular disease. The detailed mechanisms of how testosterone functions in health and disease, however, remain unclear. During the past several decades, the successful cloning of the androgen receptor (AR) and its coregulators and establishment of AR transgenic and knockout animal models have led to rapid development in this field of study. The two thematic reviews in this issue of the Journal of Endocrinology provide a timely and useful guide and source of information to discuss the current knowledge of the metabolic and vascular actions of testosterone involvement in these androgen-related disorders. They described the mechanisms of relationships between testosterone and metabolic disease and how testosterone regulates vascular function and inflammation with a comprehensive summary of updated androgen-AR findings. As more research and clinical trials have put efforts into the study of how testosterone functions in these diseases, it is expected that the roles of testosterone and its actions will become clearer in the near future.
