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Antonia Giacco, Teresa Peluso, Federica Cioffi, Stefania Iervolino, Giovanna Mercurio, Luca Roberto, Carla Reale, Marco Colella, Mario De Felice, Maria Moreno, Concetta Ambrosino, and Elena Silvestri

indispensable quartet of transcription factors defining, in humans and mice, the early thyroid development ( De Felice & Di Lauro 2004 , Park & Chatterjee 2005 ), as well as the development of specific extrathyroidal tissues ( Fernández et al. 2015 ). Based

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M M Conradie, H de Wet, D D R Kotze, J M Burrin, F S Hough, and P A Hulley

fields were examined in each section from five rats per group at 250 × magnification. Caspase activity Apoptosis in vitro was confirmed in these cells by the detection of a caspase-cleaved substrate, using an antibody

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Ryo Morimoto, Fumitoshi Satoh, Osamu Murakami, Takuo Hirose, Kazuhito Totsune, Yutaka Imai, Yoichi Arai, Takashi Suzuki, Hironobu Sasano, Sadayoshi Ito, and Kazuhiro Takahashi

). Figure 5 Reverse transcription PCR of adrenomedullin 2/intermedin, calcitonin receptor-like receptor, receptor activity-modifying proteins 1, 2, and 3 mRNA in cortisol-producing adenomas, aldosterone-producing adenomas, non-functioning adenoma

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Kotaro Horiguchi, Motoshi Kikuchi, Kenji Kusumoto, Ken Fujiwara, Tom Kouki, Kotaro Kawanishi, and Takashi Yashiro

) diluted to 1:200 and were washed with PBS again. Sections were scanned using a confocal laser microscope. Proliferation assay To visualize the proliferative activities of cells, the nucleotide analog 5-bromo-2′-deoxyuridine (BrdU, Sigma–Aldrich Corp.) was

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A V Sirotkin, P Sanislo, H-J Schaeffer, I Florkovičová, J Kotwica, J Bulla, and L Hetényi

on megacaryocytes has been demonstrated ( Sauer et al. 2001 ). The aims of this study were (1) to determine whether TPO can regulate the proliferation, apoptosis and secretory activity of ovarian cells and (2) to identify the possible

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J G Miquet, A I Sotelo, F P Dominici, M S Bonkowski, A Bartke, and D Turyn

transcriptional activators STAT5a, STAT5b and other intracellular signaling molecules ( Carter-Su et al. 2000 , Zhu et al. 2001 ). Many studies have established STAT5 as a key intracellular mediator of GH action, and STAT5b as the principal regulator of the

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Nasser Al-Shanti and Claire E Stewart

confirmed by increased creatine kinase (CK) activity and morphological differentiation, which was indicated by myotube formation. We have also examined the effect of PD98059 not only on the expression levels of myogenic transcriptional factor mRNAs (myogenin

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Eleftheria Diakogiannaki, Hannah J Welters, and Noel G Morgan

transcription factor 4 (ATF4), GRP78 (Santa Cruz), eukaryotic initiation factor 2α (eIF2α), p-eIF2α (Cell Signalling), CHOP-10, β-actin, histone H3 (Sigma). The dilution used in all cases was 1:1000. Incubation lasted for 4 h at room temperature. The membrane

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RC Fowkes and JM Burrin

Steroidogenic factor-1 (SF-1) is a key regulator of endocrine development, and mediates expression of gonadotrophin-specific genes in the pituitary. Basal and hormone stimulated transcription of the human glycoprotein hormone alpha-subunit gene (alphaGSU) in gonadotrophs involves SF-1 and its cognate binding site, the gonadotroph-specific element (GSE). In this study, we demonstrate that SF-1 significantly enhances basal and forskolin-stimulated transcription of the human alphaGSU promoter in GH(3) cells. Mutation of the GSE abolished the SF-1-mediated transactivation of basal alphaGSU promoter activity, and significantly attenuated the forskolin effect by 50%. Mutation of the Ser203 residue in SF-1 to Ala blocked basal transactivation of alphaGSU promoter activity, and halved the forskolin effect. These data collectively reveal a direct role for SF-1 and the GSE in mediating basal and forskolin-stimulated transcription of the human alphaGSU promoter in GH(3) cells. The phosphorylation site at Ser203 appears to be required for these effects.

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M Karin and L Chang

More than a decade ago our view of gene regulation by glucocorticoids (GC) and other steroid hormones underwent a dramatic change with the discovery of negative crosstalk (transcriptional interference) between the GC receptor (GCR) and transcription factor AP-1 (Jun:Fos). It was initially observed that induction of the collagenase type 1 gene, which is mediated through activation of AP-1 by growth factors and inflammatory cytokines, is repressed by GC. This repression was attributed to mutual negative interactions between AP-1 and GCR. Although the exact molecular mechanism underlying this particular case of transcriptional interference is yet to be determined, it has become clear that this and analogous interactions with other transcription factors (e.g. nuclear factor-kappaB) underlie the anti-inflammatory and immunosuppressive activity of GC. Recent studies conducted at the whole animal level indicate that the interactions between the AP-1 and GC signaling pathways are much more extensive. AP-1-related signaling via the Jun N-terminal kinases can lead to increased levels of circulating GC, which eventually down-modulate AP-1 activity via transcriptional interference. This negative feedback loop is likely to be of great importance for maintenance of homeostasis and regulation of stress responses, including acute and chronic inflammation.