| Name | estrogen receptor |
|---|---|
| Synonyms | ER; ERA; ER alpha; ERalpha; ESR; ESR 1; ESR1; ESRA… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16724547 | Li HF, Zhang P, Tian ZF, Qiu XQ, Zhang YF, Wu JX, Jia ZJ: Differential mechanisms involved in effects of and 17- on porcine coronary arteries. Pharmazie. 2006 May;61(5):461-5. The relaxations induced by and 17- were unaffected by the estrogen receptor antagonist tamoxifen, the inhibitor of prostanoid synthesis indomethacin and the protein synthesis inhibitor, cycloheximide. |
31(0,1,1,1) | Details |
| 17173074 | Ma Y, Cress WD: Transcriptional upregulation of p57 (Kip2) by the cyclin-dependent kinase inhibitor BMS-387032 is E2F dependent and serves as a negative feedback loop limiting cytotoxicity. Oncogene. 2007 May 24;26(24):3532-40. Epub 2006 Dec 18. An E2F1-estrogen receptor fusion protein activated the endogenous p57 promoter in response to hydroxytamoxifen treatment in the presence of cycloheximide. |
31(0,1,1,1) | Details |
| 15870696 | Reid G, Metivier R, Lin CY, Denger S, Ibberson D, Ivacevic T, Brand H, Benes V, Liu ET, Gannon F: Multiple mechanisms induce transcriptional silencing of a subset of genes, including oestrogen receptor alpha, in response to deacetylase inhibition by and trichostatin A. Oncogene. 2005 Jul 21;24(31):4894-907. Concomitant treatment with cycloheximide prevented most of these changes in gene expression, including downregulation of ERalpha mRNA, indicating that a limited number of genes signal a hyperacetylated state within cells. |
11(0,0,1,6) | Details |
| 19711044 | Yum J, Jeong HM, Kim S, Seo JW, Han Y, Lee KY, Yeo CY: PKA-mediated stabilization of FoxH1 negatively regulates ERalpha activity. Mol Cells. 2009 Jul;28(1):67-71. Epub 2009 Jul 8. |
9(0,0,0,9) | Details |
| 18787018 | Adams BD, Claffey KP, White BA: Argonaute-2 expression is regulated by epidermal growth factor receptor and mitogen-activated protein kinase signaling and correlates with a transformed phenotype in breast cancer cells. Endocrinology. 2009 Jan;150(1):14-23. Epub 2008 Sep 11. ERalpha-positive (ERalpha+) breast cancer cell lines, and in ERalpha (-) breast tumors. Half-life studies using cycloheximide indicated that EGF enhanced, whereas U0126 decreased, Ago2 protein stability. |
4(0,0,0,4) | Details |
| 17951260 | Kipp JL, Kilen SM, Woodruff TK, Mayo KE: Activin regulates estrogen receptor gene expression in the mouse ovary. . J Biol Chem. 2007 Dec 14;282(50):36755-65. Epub 2007 Oct 19. Activin A stimulation of ER expression was a direct effect at the level of gene transcription, as it was not abolished by cycloheximide but was abolished by actinomycin D, and in transfected granulosa cells activin A stimulated ERalpha promoter activity. |
4(0,0,0,4) | Details |
| 18417718 | Lee MJ, Lin H, Liu CW, Wu MH, Liao WJ, Chang HH, Ku HC, Chien YS, Ding WH, Kao YH: Octylphenol stimulates resistin gene expression in 3T3-L1 adipocytes via the estrogen receptor and extracellular signal-regulated kinase pathways. Am J Physiol Cell Physiol. 2008 Jun;294(6):C1542-51. Epub 2008 Apr 16. The basal half-life of resistin protein induced by cycloheximide was lengthened by octylphenol treatment, suggesting that octylphenol decreases the rate of resistin protein degradation. |
3(0,0,0,3) | Details |
| 17683929 | Pawlak KJ, Wiebe JP: Regulation of estrogen receptor (ER) levels in MCF-7 cells by metabolites. J Steroid Biochem Mol Biol. 2007 Nov-Dec;107(3-5):172-9. Epub 2007 Jun 22. Treatment with cycloheximide or actinomycin D indicated that both transcription and translation are involved in 5alphaP and 3alphaHP action on ER numbers. |
3(0,0,0,3) | Details |
| 15837795 | Beischlag TV, Perdew GH: ER alpha-AHR-ARNT protein-protein interactions mediate -dependent transrepression of dioxin-inducible gene transcription. J Biol Chem. 2005 Jun 3;280(22):21607-11. Epub 2005 Apr 18. Both AHR and ARNT were capable of interacting directly with ER alpha, as ascertained by glutathione S-transferase pull-down. 17Beta- repressed TCDD-activated Cyp1a1 and Cyp1b1 gene transcription in MCF-7 cells in the presence of cycloheximide, as determined by reverse transcription/real-time PCR. |
85(1,1,1,5) | Details |
| 18068743 | Wong CM, Tsang SY, Yao X, Chan FL, Huang Y: Differential effects of and on channels expressed in Xenopus oocytes. Steroids. 2008 Mar;73(3):272-9. Epub 2007 Nov 4. RESULTS: Both 17beta- and BSA-conjugated 17beta- increased the BK (Ca) current in a concentration-dependent manner and this effect was abolished by tetraethylammonium ions and iberiotoxin (putative BK (Ca) channel blockers). 17beta--stimulated increase in the BK (Ca) current was unaffected by treatment with ICI 182,780 (classic estrogen receptor antagonist), tamoxifen (estrogen receptor agonist/antagonist), actinomycin D (RNA synthesis inhibitor), or cycloheximide (protein synthesis inhibitor). |
31(0,1,1,1) | Details |
| 19264808 | Wickramasinghe NS, Manavalan TT, Dougherty SM, Riggs KA, Li Y, Klinge CM: downregulates miR-21 expression and increases miR-21 target gene expression in MCF-7 breast cancer cells. Nucleic Acids Res. 2009 May;37(8):2584-95. Epub 2009 Mar 5. The E (2)-induced reduction in miR-21 was inhibited by 4-hydroxytamoxifen (4-OHT), ICI 182 780 (Faslodex), and siRNA ER alpha indicating that the suppression is ER alpha-mediated. |
4(0,0,0,4) | Details |
| 17986456 | Bourdeau V, Deschenes J, Laperriere D, Aid M, White JH, Mader S: Mechanisms of primary and secondary target gene regulation in breast cancer cells. Nucleic Acids Res. 2008 Jan;36(1):76-93. Epub 2007 Nov 5. Estrogen receptors (ERs), which mediate the proliferative action of estrogens in breast cancer cells, are ligand-dependent transcription factors that regulate expression of their primary target genes through several mechanisms. To better characterize the mechanisms of gene regulation by estrogens, we have identified more than 700 putative primary and about 1300 putative secondary target genes of in MCF-7 cells through microarray analysis performed in the presence or absence of the translation inhibitor cycloheximide. |
3(0,0,0,3) | Details |
| 18450422 | Park S, Song J, Joe CO, Shin I: Akt stabilizes estrogen receptor alpha with the concomitant reduction in its transcriptional activity. Cell Signal. 2008 Jul;20(7):1368-74. Epub 2008 Mar 19. Cycloheximide decay assays and studies with proteasome inhibitor indicated that Akt1-mediated up-regulation of ERalpha was maintained by inhibiting proteasome-mediated degradation of ERalpha. |
89(1,1,1,9) | Details |
| 17609434 | Grisouard J, Medunjanin S, Hermani A, Shukla A, Mayer D: Glycogen synthase kinase-3 protects estrogen receptor alpha from proteasomal degradation and is required for full transcriptional activity of the receptor. Mol Endocrinol. 2007 Oct;21(10):2427-39. Epub 2007 Jul 3. Indeed, under this condition, ERalpha protein was rescued using the proteasome inhibitor MG132 in presence of the protein synthesis inhibitor cycloheximide. |
40(0,1,1,10) | Details |
| 19117054 | Karmakar S, Foster EA, Smith CL: downregulation of the tumor suppressor gene BTG2 requires estrogen receptor-alpha and the REA corepressor. Int J Cancer. 2009 Apr 15;124(8):1841-51. Depletion of ERalpha by siRNA indicated that the receptor is required for E2 down regulation of BTG2 mRNA levels, and cycloheximide experiments indicated that the effect of E2 on BTG2 expression was independent of intermediary protein synthesis. |
35(0,1,1,5) | Details |
| 16238455 | Li HF, Tian ZF, Qiu XQ, Wu JX, Zhang P, Jia ZJ: A study of mechanisms involved in vasodilatation induced by in isolated porcine coronary artery. Physiol Res. 2006;55(4):365-72. Epub 2005 Oct 17. However, the relaxation induced by was unaffected by the estrogen receptor antagonist tamoxifen, the inhibitor of prostanoid synthesis indomethacin, the antagonist of beta-adrenoceptors or the protein synthesis inhibitor, cycloheximide. |
31(0,1,1,1) | Details |
| 16585197 | Amlal H, Faroqui S, Balasubramaniam A, Sheriff S: up-regulates neuropeptide Y Y1 receptor expression in a human breast cancer cell line. Cancer Res. 2006 Apr 1;66(7):3706-14. To investigate this possibility, we used estrogen receptor-positive (ER+) human breast carcinoma cell line, MCF-7, and examined the effect of on Y1R gene expression and its signaling pathways. Cycloheximide decreased basal Y1R mRNA expression; however, it did not affect its increase by |
3(0,0,0,3) | Details |
| 16740979 | Chen YH, Lee MJ, Chang HH, Hung PF, Kao YH: 17 beta- stimulates resistin gene expression in 3T3-L1 adipocytes via the estrogen receptor, extracellularly regulated kinase, and CCAAT/enhancer binding protein-alpha pathways. Endocrinology. 2006 Sep;147(9):4496-504. Epub 2006 Jun 1. Treatment with either actinomycin D or cycloheximide prevented E2-stimulated resistin mRNA expression, suggesting that the effect of E2 requires new mRNA and protein synthesis. |
3(0,0,0,3) | Details |
| 17599377 | Khan S, Liu S, Stoner M, Safe S: Cobaltous chloride and hypoxia inhibit aryl hydrocarbon receptor-mediated responses in breast cancer cells. Toxicol Appl Pharmacol. 2007 Aug 15;223(1):28-38. Epub 2007 May 25. Cotreatment of ZR-75 cells with TCDD plus the protein synthesis inhibitor cycloheximide for 6 h enhanced CYP1A1 expression in cells grown under hypoxia and normoxia. The aryl hydrocarbon receptor (AhR) is expressed in estrogen receptor (ER)-positive ZR-75 breast cancer cells. |
2(0,0,0,2) | Details |
| 16322326 | O'Donnell AJ, Macleod KG, Burns DJ, Smyth JF, Langdon SP: Estrogen receptor-alpha mediates gene expression changes and growth response in ovarian cancer cells exposed to Endocr Relat Cancer. 2005 Dec;12(4):851-66. Inhibition of de novo protein synthesis by cycloheximide was used to distinguish between primary and secondary target genes regulated by E (2). |
2(0,0,0,2) | Details |
| 15857754 | Laios I, Journe F, Nonclercq D, Vidal DS, Toillon RA, Laurent G, Leclercq G: Role of the proteasome in the regulation of estrogen receptor alpha turnover and function in MCF-7 breast carcinoma cells. J Steroid Biochem Mol Biol. 2005 Mar;94(4):347-59. |
2(0,0,0,2) | Details |
| 17599049 | Hao H, d'Alincourt-Salazar M, Kelley KM, Shatnawi A, Mukherjee S, Shah YM, Ratnam M: -induced and TAFII30-mediated gene repression by direct recruitment of the estrogen receptor and co-repressors to the core promoter and its reversal by tamoxifen. Oncogene. 2007 Dec 13;26(57):7872-84. Epub 2007 Jun 25. |
2(0,0,0,2) | Details |
| 15585354 | Freyberger A, Schmuck G: Screening for estrogenicity and anti-estrogenicity: a critical evaluation of an MVLN cell-based transactivation assay. Toxicol Lett. 2005 Jan 15;155(1):1-13. Similar results were observed for cycloheximide, quabain, and other effectors of cell function. This issue initiated intense research over the past years with a focus on interactions with the estrogen receptor (ER) as for several natural and anthropogenic compounds an estrogenic potential could be demonstrated. |
2(0,0,0,2) | Details |
| 18206364 | Bollmann J, Ortmann O, Treeck O: Expression of differentiation-associated gene icb-1 is -responsive in ovarian and breast cancer cell lines. J Steroid Biochem Mol Biol. 2008 Mar;109(1-2):16-21. Epub 2007 Dec 7. Upregulation of icb-1 transcript levels was also observed after treatment with specific ERalpha-agonist PPT and was inhibited by co-treatment with pure antiestrogen ICI 182,780 in MCF-7 and OVCAR-3 ovarian cancer cells. Treatment with cycloheximide totally inhibited effects suggesting that activation of icb-1 gene expression is no ERE-dependent early response but a secondary event requiring protein synthesis. |
2(0,0,0,2) | Details |
| 19151744 | Liu HY, Wang ZM, Bai Y, Wang M, Li Y, Wei S, Zhou QH, Chen J: Different BAG-1 isoforms have distinct functions in modulating chemotherapeutic-induced apoptosis in breast cancer cells. Acta Pharmacol Sin. 2009 Feb;30(2):235-41. Epub 2009 Jan 19. In the detection of the expression of K-ras, Hsp70, cytochrome c, Raf-1, ER-alpha, and Bcl-2 in MCF-7 cells by Western blot, only Bcl-2 protein expression was significantly increased in MCF-7 cells transfected with BAG-1 p50 and p46, respectively. The mechanism by which BAG-1 affected the function of Bcl-2 was exploredby using the cycloheximide chase assay. |
1(0,0,0,1) | Details |
| 17416199 | Choi EM: increases osteoblastic differentiation and inhibits tumor necrosis factor-alpha-induced production of interleukin-6 and in osteoblastic MC3T3-E1 cells. Pharmazie. 2007 Mar;62(3):216-20. Due to their ability to bind the estrogen receptor, these compounds have the potential to counteract the deleterious effects of deficiency on bone. The effect of in increasing ALP activity and collagen content was completely prevented by the presence of 10 (-6) M cycloheximide and 10-6 M tamoxifen, suggesting that apigenin's effect results from a newly synthesized protein component and might be partly involved in action. |
1(0,0,0,1) | Details |
| 16690804 | Harrington WR, Sengupta S, Katzenellenbogen BS: regulation of the glucuronidation enzyme UGT2B15 in estrogen receptor-positive breast cancer cells. Endocrinology. 2006 Aug;147(8):3843-50. Epub 2006 May 11. UGT2B15 stimulation by is blocked by the antiestrogen ICI182,780, but not by the translational inhibitor cycloheximide, indicating that UGT2B15 is likely a primary transcriptional response mediated through the ER. |
2(0,0,0,2) | Details |
| 19499261 | Frische T, Faust M, Meyer W, Backhaus T: Toxic masking and synergistic modulation of the estrogenic activity of chemical mixtures in a yeast screen (YES). Environ Sci Pollut Res Int. 2009 Jul;16(5):593-603. Epub 2009 Jun 5. DISCUSSION: The modified YES proved to be a reliable system for the simultaneous quantification of yeast toxicity and estrogen receptor activation. Mercury, two organic solvents (DMSO) and 2,4-dinitroaniline), a surfactant (LAS-12) and the antibiotic cycloheximide were selected as toxic but non-estrogenic test chemicals. |
1(0,0,0,1) | Details |
| 16675452 | Chou YT, Yang YC: Post-transcriptional control of Cited2 by transforming growth factor beta. J Biol Chem. 2006 Jul 7;281(27):18451-62. Epub 2006 May 4. Pharmacologic inhibition of translation with cycloheximide attenuated Cited2 down-regulation by TGF-beta. Cited2 interacts with cAMP-responsive element-binding protein-binding protein (CBP)/p300, TFAP2, Lhx2, and nuclear receptors, such as peroxisome proliferator-activated receptor and estrogen receptor to function as a transcriptional modulator. |
1(0,0,0,1) | Details |
| 16042770 | Perusquia M, Navarrete E: Evidence that 17alpha- is biologically active in the uterine tissue: antiuterotonic and antiuterotrophic action. Reprod Biol Endocrinol. 2005 Jul 21;3:30. CONCLUSION: 17alpha- induces a relaxing effect, which may be independent of the classical estrogen receptor, nongenomic action, apparently mediated by inactivation of VOCCs. 17alpha- is also a weak agonist (uterotrophic response); likewise, 17alpha- may act as an antiestrogen (antiuterotrophic response). To examine the mechanism of 17alpha- action, its effect was studied in presence of beta2-antagonist antiestrogens (tamoxifen and ICI 182,780) or inhibitors of protein synthesis (cycloheximide) and transcription (actinomycin D). |
1(0,0,0,1) | Details |
| 16137569 | Arnold S: suppresses the impact of deprivation on astrocytic levels and signaling independently of the nuclear estrogen receptor. Neurobiol Dis. 2005 Oct;20(1):82-92. Re-addition of led to a rapid drop of [Ca2+] i, yet [Ca2+] i did not fully recover to the low levels recorded prior to deprivation and, moreover, astrocytic Ca2+ signaling was impaired: 5'- (ATP) and 5'- (UTP) were no longer able to trigger a transient Ca2+ response as recorded in controls. 17beta- protected astrocytes from the deprivation-induced [Ca2+] i increase and the impaired signaling independently of the nuclear estrogen receptor, as the antiestrogen tamoxifen and the protein synthesis inhibitor cycloheximide did not impede the protective effect of 17beta- |
1(0,0,0,1) | Details |
| 17009105 | Skliris GP, Lewis A, Emberley E, Peng B, Weebadda WK, Kemp A, Davie JR, Shiu RP, Watson PH, Murphy LC: Estrogen receptor-beta regulates psoriasin (S100A7) in human breast cancer. Breast Cancer Res Treat. 2007 Jul;104(1):75-85. Epub 2006 Sep 29. This induction still occurred after stable down-regulation of ERalpha using siRNA in ERbeta inducible cells. E2 increased psoriasin/S100A7 mRNA but cycloheximide treatment inhibited this effect. |
1(0,0,0,1) | Details |
| 16967517 | Zhang X, Christenson LK, Nothnick WB: Regulation of MMP-9 expression and activity in the mouse uterus by Mol Reprod Dev. 2007 Mar;74(3):321-31. Gelatin zymography revealed that E (2) alone or in combination with P (4) increased MMP-9 activation, whereas Northern analysis showed that E (2) decreased MMP-9 steady state mRNA expression and an estrogen receptor antagonist ICI-182, 780 blocked this effect. Pretreatment with a transcription inhibitor actinomycin D or translation inhibitor cycloheximide indicates that E (2) regulates uterine MMP-9 at multiple points, involving transcriptional and posttranscriptional control as well as modulation of inhibitor activities. |
1(0,0,0,1) | Details |
| 17158932 | Li C, Wu RC, Amazit L, Tsai SY, Tsai MJ, O'Malley BW: Specific amino acid residues in the basic helix-loop-helix domain of SRC-3 are essential for its nuclear localization and proteasome-dependent turnover. Mol Cell Biol. 2007 Feb;27(4):1296-308. Epub 2006 Dec 11. SRC-3/AIB1/ACTR/pCIP/RAC3/TRAM-1 is a primary transcriptional coactivator for the estrogen receptor. SRC-3 shows a time-dependent decay in the presence of cycloheximide which is not apparent for the cytoplasmic mutant. |
1(0,0,0,1) | Details |
| 18974150 | Chan CS, Song JS: CCCTC-binding factor confines the distal action of estrogen receptor. . Cancer Res. 2008 Nov 1;68(21):9041-9. The proposed method combines a recent map of the insulator protein CCCTC-binding factor (CTCF) with previous ER location studies and expression profiling in the presence of the translation inhibitor cycloheximide, providing evidence that CTCF partitions the human genome into distinct ER-regulatory blocks. |
1(0,0,0,1) | Details |
| 17962383 | Denger S, Bahr-Ivacevic T, Brand H, Reid G, Blake J, Seifert M, Lin CY, May K, Benes V, Liu ET, Gannon F: Transcriptome profiling of -regulated genes in human primary osteoblasts reveals an osteoblast-specific regulation of the insulin-like growth factor binding protein 4 gene. Mol Endocrinol. 2008 Feb;22(2):361-79. Epub 2007 Oct 25. (E2) is believed to modulate physiological functions relevant to osteoblast biology through the actions of estrogen receptors (ERs) that in turn regulate the expression of target genes. Of approximately 54,000 gene probes surveyed in this study, a total of 375 genes were up-regulated and 418 genes were down-regulated on exposure to E2, with only 46 of these being direct target genes after 24 h, as determined by concomitant cycloheximide treatment. |
1(0,0,0,1) | Details |
| 15935340 | Takada H, Hattori D, Kitayama A, Ueno N, Taira M: Identification of target genes for the Xenopus Hes-related protein XHR1, a prepattern factor specifying the midbrain-hindbrain boundary. Dev Biol. 2005 Jul 1;283(1):253-67. Among the newly identified candidate target genes of XHR1 were Enhancer of split-related genes (ESR1, ESR3/7, and ESR9) and Xenopus laevis cleavage 2 (XLCL2). XHR1-VP16-GR induced the expression of the ESR genes and XLCL2 as well as Xdelta1, Xngnr1, and XHR1 itself in the presence of DEX even after pretreatment with the protein synthesis inhibitor, cycloheximide. |
1(0,0,0,1) | Details |
| 20237589 | Hill BJ, Gebre S, Schlicker B, Jordan R, Necessary S: Nongenomic inhibition of coronary constriction by 17beta- and Can J Physiol Pharmacol. 2010 Feb;88(2):147-52. The protein synthesis inhibitor cycloheximide and the estrogen receptor antagonists ICI 182780 and tamoxifen did not affect the attenuation. |
0(0,0,0,0) | Details |
| 18775847 | Gui Y, Zheng XL, Zheng J, Walsh MP: Inhibition of rat aortic smooth muscle contraction by . Am J Physiol Heart Circ Physiol. 2008 Nov;295(5):H1935-42. Epub 2008 Sep 5. The inhibitory effects of 2-ME and E2 were not affected by ICI-182780 (an estrogen receptor antagonist) or actinomycin D (a gene transcription inhibitor); however, the effect of 2-ME, but not E2, was prevented by cycloheximide (a protein synthesis inhibitor). |
0(0,0,0,0) | Details |