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Haruo Nogami, Yoshiki Hiraoka, Kiyomoto Ogasawara, Sadakazu Aiso and Setsuji Hisano

prolactin gene. Molecular Endocrinology 2 1374 –1381. Korytko AI & Cuttler L 1997 Thyroid hormone and glucocorticoid regulation of pituitary growth hormone-releasing hormone receptor gene expression. Journal of

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Y Kazeto and J M Trant

). Therefore, the precise regulation of E 2 biosynthesis, controlled primarily through the expression of genes encoding steroidogenic enzymes, is apparently required for reproductive success. Cytochrome P450 aromatase (CYP19) is the terminal steroidogenic

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Edson F Nogueira, Yewei Xing, Claudia A V Morris and William E Rainey

confirm the studies performed by Romero et al . (2004) , who have also studied Ang II responsive genes in H295R cells. In the present study, we examined the role of these transcription factors in the regulation of the enzymes involved in adrenal

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A Al Kahtane, Y Chaiseha and M El Halawani

It is well documented that prolactin (PRL) release and PRL gene expression in birds are controlled by the tonic stimulation of hypothalamic vasoactive intestinal peptide (VIP). However, there is good evidence that dopamine (DA) exerts both stimulatory (at the hypothalamic level) and inhibitory (at the pituitary level) effects on PRL secretion. The interactions between VIP and DA in the regulation of PRL gene transcription are not known. This study was designed to examine the effects of a D(2) DA receptor agonist (D(2)AG; R(-)-propylnorapomorphine HCl) on basal and VIP-stimulated PRL gene transcription rate, PRL mRNA steady-state levels, PRL mRNA stability and PRL release from cultured turkey anterior pituitary cells. The D(2)AG (10(-)(10) M) completely inhibited the stimulatory effect of VIP (10(-)(7) M) upon nascent PRL mRNA as determined utilizing a nuclear run-on transcription assay. To examine further the effect of the D(2)AG on PRL mRNA post-transcriptional events, anterior pituitary cells were treated with different concentrations of D(2)AG (10(-)(12)-10(-)(4) M). Semi-quantitative RT-PCR and RIA were performed to determine the levels of PRL mRNA and PRL content in the medium respectively. The results show that D(2)AG inhibited VIP-stimulated PRL mRNA steady-state levels as well as basal and VIP-stimulated PRL release, effects which were diminished by the D(2) DA receptor antagonist, S(-)-eticlopride HCl (10(-)(10) M). Actinomycin D (5 microg/ml), an inhibitor of mRNA synthesis, was used to assess the effect of D(2)AG on PRL mRNA stability in response to VIP. The stimulatory effect of VIP on PRL mRNA stability was completely negated by the D(2)AG (from a half-life of 53.0+/-2.3 h in VIP-treated cells to 25.5+/-1.6 h in D(2)AG+VIP-treated cells, P<or=0.05). These results support the hypothesis that VIP and DA play a major role in the regulation of PRL gene expression in avian species, at both the transcriptional and post-transcriptional levels. In addition, these findings suggest that the DAergic system inhibits PRL release and synthesis by antagonizing VIP at the pituitary level via D(2) DA receptors.

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E Yamamori, M Asai, M Yoshida, K Takano, K Itoi, Y Oiso and Y Iwasaki

hypothalamus, is known to play a pivotal role in the regulation of the HPA axis because it serves as a major regulator of the synthesis and secretion of adrenocorticotropin by the pituitary ( Vale et al. 1981 ). In fact, genetic ablation of the CRH gene

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J G Moggs, T C Murphy, F L Lim, D J Moore, R Stuckey, K Antrobus, I Kimber and G Orphanides

on breast epithelial cells are mediated, at least in part, via the altered expression of genes involved in cell cycle regulation ( Prall et al. 1997 ). Transcriptional regulation of estrogen-responsive genes is mediated by two members of the nuclear

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SL Samson and NC Wong

Sp1 is a ubiquitous nuclear factor that plays a key role in maintaining basal transcription of 'house-keeping' genes. However, recent evidence points to a more important function for Sp1 in mediating 'cross-talk' between selected signaling cascades to regulate the target genes that respond to these pathways. The role of Sp1 in mediating the actions of the peptide hormone insulin is of specific interest and serves as a model for detailing effects of intracellular signaling on Sp1 activity. This review summarizes studies suggesting that changes in Sp1 phosphorylation provide one potential mechanism for manipulating activity of this protein. A growing body of evidence reveals that the DNA binding and transcription activity of Sp1 may increase or decrease in response to changes in phosphorylation. This enables 'fine-tuning' of Sp1 activity for regulation of gene transcription. Several mechanisms exist by which Sp1 alters gene activity in response to insulin. These include independent Sp1 activity as well as collaboration or competition with others factors. This review points to an ever-increasing role for Sp1 in regulating the transcription of genes in response to extracellular signals such as insulin.

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Bogusz Trojanowicz, Anja Winkler, Kathrin Hammje, Zhouxun Chen, Carsten Sekulla, Dagobert Glanz, Cornelia Schmutzler, Birgit Mentrup, Sabine Hombach-Klonisch, Thomas Klonisch, Rainer Finke, Josef Köhrle, Henning Dralle and Cuong Hoang-Vu

, many of MYC targeting pathways are deregulated in cancer cells and contribute to its enhanced expression ( Vervoorts et al . 2006 ). In order to clarify the relationship between RA-mediated down-regulation of ENO1 gene products and reduced

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J C Pascall

Steroid hormones generally mediate their effects by interacting with specific receptors which then bind to defined DNA sequences in the regulatory regions of target genes to activate expression (see Gronmeyer (1992) and references therein). However, the post-transcriptional regulation of gene expression by steroid hormones is also well documented (see Nielsen & Shapiro 1990). Indeed steroid hormones were amongst the first agents to be demonstrated to play a role in mRNA stabilization (Palmiter & Carey 1974). For example, glucocorticoid hormones have been shown to enhance the stability of growth hormone mRNA (Paek & Axel 1987), testosterone has been reported to induce changes in the poly(A) tail length of the mRNA encoding cystatin-related protein (Vercaeren et al. 1992) and testosterone and/or oestrogen induce changes in the poly(A) tail length of the vasopressin mRNA (Carter & Murphy 1993) associated with changes in mRNA accumulation. However, it is still unclear how steroids mediate these

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Hannah E Lapp, Andrew A Bartlett and Richard G Hunter

observed for several metabolic, inflammatory and neuroendocrine-related genes. These findings provided direct evidence for mitochondrial regulation of the peripheral endocrine acute stress response as well as regulatory effects on efferent brain targets of