The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Chemical Compound Review

AC1NR4TH     N-butyl-11- [(8S,9S,13S,14S,17S)-3,17...

Synonyms:
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of Ici 164384

 

High impact information on Ici 164384

 

Chemical compound and disease context of Ici 164384

 

Biological context of Ici 164384

 

Anatomical context of Ici 164384

  • ICI 164384 had no effect on the two respective parental cell lines, CEM/CCRF and H69 P [2].
  • The compound ICI 164384 was devoid of oestrogenic activity in the uterus and vagina of both species and on the hypothalamic-pituitary axis of the rat [10].
 

Gene context of Ici 164384

  • In addition, the ER alpha antagonist ICI-164384 is a potent antagonist for ER beta as well [11].
  • The antiestrogen ICI 164384 also transiently decreased the steady state mRNA levels of both IGFBP 4 and IGFBP 5 [12].
  • This is the first report on repression of components of the extracellular matrix by estradiol and induction by the complete antiestrogen ICI 164384 [13].
  • In contrast, the presence of ICI 164384, which does not induce the selection of resistant subclones under the same experimental conditions in which TAM does, may improve the efficacy of low concentration of beta-IFN and prevent the development of a secondary TAM-induced resistance [14].
  • Pretreatment of MCF-7 cells for 2 days with either OH TAM or ICI 164384 did not inhibit EGF-induced increases in cell proliferation [15].

References

  1. Points of action of estrogen antagonists and a calmodulin antagonist within the MCF-7 human breast cancer cell cycle. Musgrove, E.A., Wakeling, A.E., Sutherland, R.L. Cancer Res. (1989) [Pubmed]
  2. Circumvention of doxorubicin resistance in multi-drug resistant human leukaemia and lung cancer cells by the pure antioestrogen ICI 164384. Hu, X.F., Nadalin, G., De Luise, M., Martin, T.J., Wakeling, A., Huggins, R., Zalcberg, J.R. Eur. J. Cancer (1991) [Pubmed]
  3. Mechanism of vascular smooth muscle relaxation by estrogen in depolarized rat and mouse aorta. Role of nuclear estrogen receptor and Ca2+ uptake. Freay, A.D., Curtis, S.W., Korach, K.S., Rubanyi, G.M. Circ. Res. (1997) [Pubmed]
  4. Differential effects of estrogen and antiestrogen on transforming growth factor gene expression in endometrial adenocarcinoma cells. Gong, Y., Ballejo, G., Murphy, L.C., Murphy, L.J. Cancer Res. (1992) [Pubmed]
  5. Inducible overexpression of cyclin D1 in breast cancer cells reverses the growth-inhibitory effects of antiestrogens. Wilcken, N.R., Prall, O.W., Musgrove, E.A., Sutherland, R.L. Clin. Cancer Res. (1997) [Pubmed]
  6. Resistance to different antiestrogens is caused by different multi-factorial changes and is associated with reduced expression of IGF receptor Ialpha. Brockdorff, B.L., Heiberg, I., Lykkesfeldt, A.E. Endocr. Relat. Cancer (2003) [Pubmed]
  7. Differential effects of retinoids and antiestrogens on cell cycle progression and cell cycle regulatory genes in human breast cancer cells. Wilcken, N.R., Sarcevic, B., Musgrove, E.A., Sutherland, R.L. Cell Growth Differ. (1996) [Pubmed]
  8. Inhibition of estrone sulfatase and 17 beta-hydroxysteroid dehydrogenase by antiestrogens. Santner, S.J., Santen, R.J. J. Steroid Biochem. Mol. Biol. (1993) [Pubmed]
  9. Synergism between a half-site and an imperfect estrogen-responsive element, and cooperation with COUP-TFI are required for estrogen receptor (ER) to achieve a maximal estrogen-stimulation of rainbow trout ER gene. Petit, F.G., Métivier, R., Valotaire, Y., Pakdel, F. Eur. J. Biochem. (1999) [Pubmed]
  10. Novel antioestrogens without partial agonist activity. Wakeling, A.E., Bowler, J. J. Steroid Biochem. (1988) [Pubmed]
  11. ER beta: identification and characterization of a novel human estrogen receptor. Mosselman, S., Polman, J., Dijkema, R. FEBS Lett. (1996) [Pubmed]
  12. Expression of insulin-like growth factor binding proteins by T-47D human breast cancer cells: regulation by progestins and antiestrogens. Coutts, A., Murphy, L.J., Murphy, L.C. Breast Cancer Res. Treat. (1994) [Pubmed]
  13. Fibronectin is an estrogen-repressed protein in RUCA-I rat endometrial adenocarcinoma cells. Vollmer, G., Hopert, A.C., Ellerbrake, N., Wünsche, W., Knuppen, R. J. Steroid Biochem. Mol. Biol. (1995) [Pubmed]
  14. The effect of ICI 164384 and beta-interferon on the growth and steroid receptor profile of breast cancer cell lines. Coradini, D., Biffi, A., Pirronello, E., Di Fronzo, G. Anticancer Res. (1995) [Pubmed]
  15. Contrasting ability of antiestrogens to inhibit MCF-7 growth stimulated by estradiol or epidermal growth factor. Cormier, E.M., Jordan, V.C. European journal of cancer & clinical oncology. (1989) [Pubmed]
 
WikiGenes - Universities