Name | glucocorticoid receptor |
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Synonyms | GCCR; GCR; GR; GRL; Glucocorticoid receptor; NR3C1; Glucocorticoid receptors |
Name | cycloheximide |
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CAS |
PubMed | Abstract | RScore(About this table) | |
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15862954 | Siriani D, Mitsiou DJ, Alexis MN: Heat-induced degradation of overexpressed glucocorticoid receptor Separate protective roles of hsp90 and hsp70. J Steroid Biochem Mol Biol. 2005 Feb;94(1-3):93-101. Epub 2005 Feb 24. About 40% of this aggregated receptor was degraded in cells recovering at 37 degrees C in the presence of cycloheximide. |
2(0,0,0,2) | Details |
15802531 | Baumann S, Dostert A, Novac N, Bauer A, Schmid W, Fas SC, Krueger A, Heinzel T, Kirchhoff S, Schutz G, Krammer PH: Glucocorticoids inhibit activation-induced cell death (AICD) via direct DNA-dependent repression of the CD95 ligand gene by a glucocorticoid receptor dimer. Blood. 2005 Jul 15;106(2):617-25. Epub 2005 Mar 31. |
2(0,0,0,2) | Details |
17026526 | Morsink MC, Joels M, Sarabdjitsingh RA, Meijer OC, De Kloet ER, Datson NA: The dynamic pattern of glucocorticoid receptor-mediated transcriptional responses in neuronal PC12 cells. J Neurochem. 2006 Nov;99(4):1282-98. Epub 2006 Oct 2. Real-time quantatitive PCR of transcripts in cycloheximide-treated cells showed that all five GR-responsive genes selected from the 1-h time point were primary responsive, whereas all four GR-responsive genes selected from the 3-h time point were downstream responsive. |
2(0,0,0,2) | Details |
16198345 | Lim WC, Park M, Bahn JJ, Inoue H, Lee YJ: Hypertonic cyclooxygenase-2 occurs independently of NF-kappaB and is inhibited by the glucocorticoid receptor in A549 cells. FEBS Lett. 2005 Oct 10;579(24):5430-6. This induction was a transcriptional event that occurred in the absence of the protein synthesis inhibitor cycloheximide and was the result of enhanced promoter activity, as examined with the use of full-length COX-2 promoter-driven reporter plasmids. |
induction of 2(0,0,0,2) | Details |
19648110 | King EM, Holden NS, Gong W, Rider CF, Newton R: Inhibition of NF-kappaB-dependent transcription by MKP-1: transcriptional repression by glucocorticoids occurring via p38 MAPK. J Biol Chem. 2009 Sep 25;284(39):26803-15. Epub 2009 Jul 31. Acting via the glucocorticoid receptor (GR), glucocorticoids exert potent anti-inflammatory effects partly by repressing inflammatory gene transcription occurring via factors such as NF-kappaB. |
1(0,0,0,1) | Details |
16428353 | Boixel C, Gavillet B, Rougier JS, Abriel H: myocytes. Am J Physiol Heart Circ Physiol. 2006 Jun;290(6):H2257-66. Epub 2006 Jan 20. In 24-h coincubation experiments, with the use of actinomycin D, cycloheximide, or brefeldin A, the effect of on I (Na) was abolished. Spironolactone (mineralocorticoid receptor antagonist, 10 microM) prevented the 1 microM -dependent I (Na) increase, whereas RU-38486 (glucocorticoid receptor antagonist, 10 microM) did not. |
increases voltage-gated current in ventricular 1(0,0,0,1) | Details |
17537407 | Barar J, Campbell L, Hollins AJ, Thomas NP, Smith MW, Morris CJ, Gumbleton M: Cell selective glucocorticoid induction of caveolin-1 and caveolae in differentiating pulmonary alveolar epithelial cell cultures. Biochem Biophys Res Commun. 2007 Jul 27;359(2):360-6. Epub 2007 May 24. Here, we show in both a primary differentiating rat alveolar culture, and a human alveolar cell line (A549) that caveolae formation and caveolin-1 expression are dependent upon dexamethasone Dex, and is inhibited by the glucocorticoid receptor (GR) antagonist, mifepristone. The actions of glucocorticoid upon caveolin-1 appear indirect acting via intermediary genes as evidenced by cycloheximide (CHX) abolition of Dex-induced increases in caveolin-1 mRNA and by recombinant transfection studies using the caveolin-1 promoter cloned upstream of a reporter gene. |
1(0,0,0,1) | Details |
19225053 | Pergher PS, Leite-Dellova D, de Mello-Aires M: Direct action of In the presence of (in similar concentration used to prepare the hormonal solution), spironolactone (10 (-6) M, a mineralocorticoid receptor antagonist), actinomycin D (10 (-6) M, an inhibitor of gene transcription), or cycloheximide (40 mM, an inhibitor of protein synthesis), the J (HCO (3)(-)) and the [Ca (2+)](i) were not different from the control value; these drugs also did not prevent the stimulatory effect of on J (HCO (3)(-)) and on [Ca (2+)](i). However, in the presence of RU 486 alone [10 (-6) M, a classic glucocorticoid receptor (GR) antagonist], a significant decrease on J (HCO (3)(-)) and on [Ca (2+)](i) was observed; this antagonist also inhibited the stimulatory effect of on J (HCO (3)(-)) and on [Ca (2+)](i). |
on reabsorption in in vivo cortical proximal tubule. Am J Physiol Renal Physiol. 2009 May;296(5):F1185-93. Epub 2009 Feb 18.1(0,0,0,1) | Details |
19162058 | Roy B, Rai U: Genomic and non-genomic effect of These membrane-bound glucocorticoid receptors seem similar to cytosolic GR, as rapid inhibitory effect of was blocked by the cytoplasmic glucocorticoid receptor blocker RU-486. |
on phagocytosis in freshwater teleost Channa punctatus: an in vitro study. Steroids. 2009 Apr-May;74(4-5):449-55. Epub 2008 Dec 31.1(0,0,0,1) | Details |
16125142 | Sugiyama T, Yoshimoto T, Hirono Y, Suzuki N, Sakurada M, Tsuchiya K, Minami I, Iwashima F, Sakai H, Tateno T, Sato R, Hirata Y: osteopontin gene expression in rat endothelial cells. Biochem Biophys Res Commun. 2005 Oct 14;336(1):163-7. The -induced osteopontin mRNA expression was completely blocked by a transcription inhibitor, actinomycin D, and a protein synthesis inhibitor, cycloheximide. |
increases 0(0,0,0,0) | Details |
19190257 | Goto J, Otsuka F, Yamashita M, Suzuki J, Otani H, Takahashi H, Miyoshi T, Mimura Y, Ogura T, Makino H: Enhancement of production by bone morphogenetic protein-4 through activating Rho and SAPK/JNK pathway in adrenomedullar cells. Am J Physiol Endocrinol Metab. 2009 Apr;296(4):E904-16. Epub 2009 Feb 3. Cycloheximide reduced both - and dexamethasone-induced TH mRNA. |
-induced catecholamine 0(0,0,0,0) | Details |
18360057 | Hayashi H, Kobara M, Abe M, Tanaka N, Gouda E, Toba H, Yamada H, Tatsumi T, Nakata T, Matsubara H: Neither an inhibitor for nuclear transcription (actinomycin D) nor an inhibitor of new protein synthesis (cycloheximide) blocked this rapid activation, and specific binding of to plasma membrane fraction was inhibited by eplerenone, suggesting a nongenomic mechanism. |
nongenomically produces oxidase-dependent reactive species and induces myocyte apoptosis. Hypertens Res. 2008 Feb;31(2):363-75.0(0,0,0,0) | Details |
18221228 | Capasso A: Glucocorticoids involvement in the control of CNS excitability. Recent Pat CNS Drug Discov. 2007 Jun;2(2):155-65. The ability of actinomicyn D and/or cycloheximide as well as of RU-38486 to block dexamethasone's effects indicates that the steroid's interference with psychostimulants-mediated effects involve a protein-synthesis-dependent mechanism via glucocorticoid receptors. |
81(1,1,1,1) | Details |
16971495 | Wang D, Zhang H, Lang F, Yun CC: Acute activation of NHE3 by dexamethasone correlates with activation of SGK1 and requires a functional glucocorticoid receptor. Am J Physiol Cell Physiol. 2007 Jan;292(1):C396-404. Epub 2006 Sep 13. Chronic regulation (24 h) of NHE3 was blocked completely by prevention of protein synthesis with cycloheximide or actinomycin D and by the glucocorticoid receptor blocker RU486. |
33(0,1,1,3) | Details |
16111661 | Komatsuzaki Y, Murakami G, Tsurugizawa T, Mukai H, Tanabe N, Mitsuhashi K, Kawata M, Kimoto T, Ooishi Y, Kawato S: Rapid spinogenesis of pyramidal neurons induced by activation of glucocorticoid receptors in adult male rat hippocampus. Biochem Biophys Res Commun. 2005 Oct 7;335(4):1002-7. Because the presence of 10 microM cycloheximide, an inhibitor of protein synthesis, did not suppress the DEX effect, these responses are probably non-genomic. |
2(0,0,0,2) | Details |
16510135 | Mulholland PJ, Self RL, Hensley AK, Little HJ, Littleton JM, Prendergast MA: A 24 h glucocorticoid receptor activation or protein synthesis. Brain Res. 2006 Apr 12;1082(1):165-72. Epub 2006 Feb 28. In contrast, 24 h exposure with the MR antagonist spironolactone (1-10 microM), the GR antagonist RU-486 (1-10 microM), or the protein synthesis inhibitor cycloheximide (1 microM) failed to reduce the significant increase in propidium iodide uptake. |
exposure exacerbates excitotoxic insult in rat hippocampal slice cultures independently of 2(0,0,0,2) | Details |
15899836 | Tran T, Shatnawi A, Zheng X, Kelley KM, Ratnam M: Enhancement of folate receptor alpha expression in tumor cells through the glucocorticoid receptor: a promising means to improved tumor detection and targeting. Cancer Res. 2005 May 15;65(10):4431-41. |
2(0,0,0,2) | Details |