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Kathrin Zopf, Kathrin R Frey, Tina Kienitz, Manfred Ventz, Britta Bauer and Marcus Quinkler

Introduction Polymorphisms of the glucocorticoid receptor (GR) may influence the sensitivity to glucocorticoids by altering the GR expression (e.g. reducing transcription) and influencing transactivation and transrepression of target genes

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Tatiana V Novoselova, Peter J King, Leonardo Guasti, Louise A Metherell, Adrian J L Clark and Li F Chan

LA Krude H Ball C O’Riordan SMP Costigan C Lynch SA Savage MO Cavarzere P Clark AJL . Homozygous nonsense and frameshift mutations of the ACTH receptor in children with familial glucocorticoid deficiency (FGD) are not associated with

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Legh Wilkinson, Nicolette J D Verhoog and Ann Louw

signalling, often resulting in various peripheral effects, one of which is the tissue-specific reductions in the glucocorticoid receptor α (GRα) functional pool. This reduction in the GRα functional pool may ultimately drive the development of acquired GC

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Fernando Aprile-Garcia, María Antunica-Noguerol, Maia Ludmila Budziñski, Ana C Liberman and Eduardo Arzt

action during inflammation (23, 24) . GCs exert their biological effects binding to the glucocorticoid receptor (GR), which is a ligand-activated TF that regulates the expression of target genes, either positively or negatively (18, 25) . In an

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Sylvia Thiele, Anke Hannemann, Maria Winzer, Ulrike Baschant, Heike Weidner, Matthias Nauck, Rajesh V Thakker, Martin Bornhäuser, Lorenz C Hofbauer and Martina Rauner

glucocorticoid-induced osteoporosis (GIO) involves many organ systems. At the skeletal level, GCs stimulate osteoclastogenesis and profoundly inhibit bone formation ( 3 , 4 ). While an increased receptor activator of NF-κB ligand (RANKL)/osteoprotegerin (OPG

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A Daniel Bird, Spencer Greatorex, David Reser, Gareth G Lavery and Timothy J Cole

in aldosterone target tissues where it prevents inappropriate activation of the mineralocorticoid receptor (MR) by glucocorticoids by efficiently converting cortisol to inactive cortisone ( 6 , 7 ). Inappropriate 11βHSD1 expression and activity is

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Greta B Raglan, Louis A Schmidt and Jay Schulkin

JL Mo M DiLeone RJ Koleske AJ Taylor JR. Action control is mediated by prefrontal BDNF and glucocorticoid receptor binding . PNAS 2012 109 20714 – 20719 . ( doi:10.1073/pnas.1208342109 ) 7 Schulkin J Morgan MA Rosen

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Trevor Lewis, Eva Zeisig and Jamie E Gaida

receptors Glucocorticoids mainly act via the cytoplasmic glucocorticoid receptor ( 22 ). Upon activation by glucocorticoid the glucocorticoid receptor undergoes a conformational change. This change triggers nuclear translocation. Inside the nucleus, the

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Janko Sattler, Jinwen Tu, Shihani Stoner, Jingbao Li, Frank Buttgereit, Markus J Seibel, Hong Zhou and Mark S Cooper

then blocked with 5% goat serum for 30 min and incubated overnight with the primary antibody for 11β-HSD1 (1:100, Cayman Chemicals) and glucocorticoid receptor (GR) (1:400, sc-1004, Santa Cruz Biotechnology). A biotinylated secondary antibody was

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Peter Ergang, Anna Mikulecká, Martin Vodicˇka, Karla Vagnerová, Ivan Mikšík and Jirˇí Pácha

merely depend on the level of the free hormone, activity of multidrug resistance efflux pumps and density of glucocorticoid receptors in target cells but also on the prereceptor metabolism of glucocorticoids, which is catalyzed by two enzymes, 11β