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According to the traditional model, steroid hormones bind to intracellular receptors and subsequently modulate transcription and protein synthesis, thus triggering genomic events finally responsible for delayed effects. Based upon similarities in molecular structure, specific receptors for steroids, vitamin D(3) derivatives, thyroid hormone, retinoids, and(More)
Steroids may exert their action in living cells by several ways: 1). the well-known genomic pathway, involving hormone binding to cytosolic (classic) receptors and subsequent modulation of gene expression followed by protein synthesis. 2). Alternatively, pathways are operating that do not act on the genome, therefore indicating nongenomic action. Although(More)
There is increasing evidence for rapid effects of steroids that are incompatible with the classical model of genomic steroid action. To address the diversity of mechanisms for rapid steroid signaling described over the past years, a classification of rapid steroid effects has been proposed to promote the discussion and understanding of nongenomic steroid(More)
In addition to the classical genomic steroid actions on modulation of transcription and protein synthesis, rapid, nongenomic effects have been described for various steroids. These effects on cellular signaling and function are supposed to be transmitted by membrane binding sites unrelated to the classical intracellular receptors. Recently, a high affinity(More)
We have cloned two human putative steroid binding membrane proteins, termed Hpr6.6 and Dg6. Hpr6.6 is the human homolog of a previously cloned porcine progesterone binding protein. Both proteins contain a putative transmembrane domain and a highly conserved stretch of 58 amino acids. Hpr6.6 mRNA is expressed predominantly in liver and kidney, whereas Dg6(More)
Aldosterone can elicit rapid nongenomic effects both in vivo and in vitro, often mediated by signal transduction cascades. However, it is not understood how these rapid effects are initiated. In this study we show that aldosterone leads to rapid activation of mitogen activated protein kinases ERK1/2 in the cortical collecting duct cell line M-1. Inhibitors(More)
A coiling-inducing factor was isolated from tendrils of Bryonia dioica Jacq. and identified by infrared, 1H-, 13C-nuclear magnetic resonance and mass spectrometry as α-linolenic acid. When applied to detached tendrils, exogenous α-linolenic acid, but not linoleic acid or oleic acid, induced tendril coiling. Further investigations showed that metabolites of(More)
Rapid, nongenomic effects of steroids are likely to be mediated by membrane receptors not by intracellular steroid receptors. We recently identified a progesterone membrane binding protein (mPR) from human liver. The corresponding hmpr gene is comprised of 3 exons and 2 introns. The promoter sequence of hmpr lacks a typical TATA box but contains instead a(More)
Rapid, nongenomic effects of steroids are supposed to be transmitted by membrane receptors unrelated to the classic intracellular steroid receptors. In this context, a putative progesterone membrane binding protein (mPR) has been identified, recently. Here we show that expression of mPR-cDNA in CHO cells leads to increased microsomal progesterone binding.(More)
The classical theory of steroid hormone action comprises binding to an intracellular receptor followed by modulation of transcriptional and translational events. These cumbersome model explains the characteristic latency of these genomic steroid effects. Over the past two decades, increasing evidence for rapid nongenomic effects of steroids, incompatible(More)