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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Chemical Compound Review

CI-920     sodium(6R)-6- [(1E,3R,4R,6R,7Z,9Z,11E)- 3,6...

Synonyms:
 
 
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Disease relevance of

 

High impact information on

  • Chromosome condensation induced by fostriecin does not require p34cdc2 kinase activity and histone H1 hyperphosphorylation, but is associated with enhanced histone H2A and H3 phosphorylation [5].
  • The treatment of these G2-arrested FT210 cells with fostriecin or okadaic acid resulted in full chromosome condensation in the absence of p34cdc2 kinase activity or histone H1 hyperphosphorylation [5].
  • Phosphorylation of CPI-17 in rabbit arteries was enhanced by calyculin A but not okadaic acid or fostriecin, consistent with PP1-mediated dephosphorylation [6].
  • In 22- to 35-day cerebellar cultures, specific inhibition of postsynaptic PP-2A by fostriecin (100 nM) or cytostatin (10-60 microM) induced a gradual and use-dependent decrease of synaptic current evoked by the stimulation of a single granule cell, without altering receptor kinetics nor passive electrical properties [7].
  • Fostriecin, an inhibitor of protein phosphatase 2A, limits myocardial infarct size even when administered after onset of ischemia [1].
 

Chemical compound and disease context of

 

Biological context of

 

Anatomical context of

 

Associations of with other chemical compounds

 

Gene context of

  • First, TNF-induced degradation of IkappaB is attenuated in cells treated with okadaic acid or fostriecin, two potent inhibitors of PP2A [21].
  • In addition, pretreatment of cells with the protein phosphatase 2A (PP2A) inhibitors okadaic acid and fostriecin increased basal and H(2)O(2)-stimulated ERK phosphorylation [22].
  • The cAMP-mediated dephosphorylation of CRHSP-24 was inhibited by low concentrations of okadaic acid (10 nM) and fostriecin (1 microM), suggesting that CRHSP-24 is regulated by PP2A or PP4 [23].
  • Test of a PP2A-specific inhibitor, fostriecin, on cells arrested in G2/M via CRK depletion or a knockdown of the PP2A catalytic subunit from the CRK-depleted cells both showed a partial lift of the G2/M block without forming multinucleate cells [24].
  • All inhibitors induced a concentration-dependent G2 delay or arrest that could be overcome with fostriecin or okadaic acid or by inactivation of RCC1 in tsBN2 cells [25].
 

Analytical, diagnostic and therapeutic context of

References

  1. Fostriecin, an inhibitor of protein phosphatase 2A, limits myocardial infarct size even when administered after onset of ischemia. Weinbrenner, C., Baines, C.P., Liu, G.S., Armstrong, S.C., Ganote, C.E., Walsh, A.H., Honkanen, R.E., Cohen, M.V., Downey, J.M. Circulation (1998) [Pubmed]
  2. Total synthesis of fostriecin (CI-920). Boger, D.L., Ichikawa, S., Zhong, W. J. Am. Chem. Soc. (2001) [Pubmed]
  3. Protein phosphatase 2A enhances activation of human immunodeficiency virus type 1 by phorbol myristate acetate. Faulkner, N.E., Lane, B.R., Bock, P.J., Markovitz, D.M. J. Virol. (2003) [Pubmed]
  4. The effects of protein phosphatase inhibitors on nociceptive behavioral responses of rats following intradermal injection of capsaicin. Zhang, X., Wu, J., Fang, L., Willis, W.D. Pain (2003) [Pubmed]
  5. Chromosome condensation induced by fostriecin does not require p34cdc2 kinase activity and histone H1 hyperphosphorylation, but is associated with enhanced histone H2A and H3 phosphorylation. Guo, X.W., Th'ng, J.P., Swank, R.A., Anderson, H.J., Tudan, C., Bradbury, E.M., Roberge, M. EMBO J. (1995) [Pubmed]
  6. Phosphoprotein inhibitor CPI-17 specificity depends on allosteric regulation of protein phosphatase-1 by regulatory subunits. Eto, M., Kitazawa, T., Brautigan, D.L. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  7. Protein phosphatase 2A inhibition induces cerebellar long-term depression and declustering of synaptic AMPA receptor. Launey, T., Endo, S., Sakai, R., Harano, J., Ito, M. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  8. Protein phosphatase inhibitors calyculin A and fostriecin protect rabbit cardiomyocytes in late ischemia. Armstrong, S.C., Gao, W., Lane, J.R., Ganote, C.E. J. Mol. Cell. Cardiol. (1998) [Pubmed]
  9. Detection of DNA strand breaks in individual apoptotic cells by the in situ terminal deoxynucleotidyl transferase and nick translation assays. Gorczyca, W., Gong, J., Darzynkiewicz, Z. Cancer Res. (1993) [Pubmed]
  10. Antitumor drug fostriecin inhibits the mitotic entry checkpoint and protein phosphatases 1 and 2A. Roberge, M., Tudan, C., Hung, S.M., Harder, K.W., Jirik, F.R., Anderson, H. Cancer Res. (1994) [Pubmed]
  11. Fostriecin-mediated G2-M-phase growth arrest correlates with abnormal centrosome replication, the formation of aberrant mitotic spindles, and the inhibition of serine/threonine protein phosphatase activity. Cheng, A., Balczon, R., Zuo, Z., Koons, J.S., Walsh, A.H., Honkanen, R.E. Cancer Res. (1998) [Pubmed]
  12. Cytostatic and cytotoxic effects of fostriecin on human promyelocytic HL-60 and lymphocytic MOLT-4 leukemic cells. Hotz, M.A., Del Bino, G., Lassota, P., Traganos, F., Darzynkiewicz, Z. Cancer Res. (1992) [Pubmed]
  13. Changes in nuclear chromatin related to apoptosis or necrosis induced by the DNA topoisomerase II inhibitor fostriecin in MOLT-4 and HL-60 cells are revealed by altered DNA sensitivity to denaturation. Hotz, M.A., Traganos, F., Darzynkiewicz, Z. Exp. Cell Res. (1992) [Pubmed]
  14. The antitumor drug fostriecin induces vimentin hyperphosphorylation and intermediate filament reorganization. Ho, D.T., Roberge, M. Carcinogenesis (1996) [Pubmed]
  15. Two modes of exocytosis from synaptosomes are differentially regulated by protein phosphatase types 2A and 2B. Baldwin, M.L., Rostas, J.A., Sim, A.T. J. Neurochem. (2003) [Pubmed]
  16. Comparative toxicity of fostriecin, hepsulfam and pyrazine diazohydroxide to human and murine hematopoietic progenitor cells in vitro. Du, D.L., Volpe, D.A., Grieshaber, C.K., Murphy, M.J. Investigational new drugs. (1991) [Pubmed]
  17. Protein phosphatase 2A and phosphoprotein SET regulate androgen production by P450c17. Pandey, A.V., Mellon, S.H., Miller, W.L. J. Biol. Chem. (2003) [Pubmed]
  18. p38 MAPK activation elevates serotonin transport activity via a trafficking-independent, protein phosphatase 2A-dependent process. Zhu, C.B., Carneiro, A.M., Dostmann, W.R., Hewlett, W.A., Blakely, R.D. J. Biol. Chem. (2005) [Pubmed]
  19. Comparison of effects of fostriecin, novobiocin, and camptothecin, inhibitors of DNA topoisomerases, on DNA replication and repair in human cells. Gedik, C.M., Collins, A.R. Nucleic Acids Res. (1990) [Pubmed]
  20. Regulators of serine/threonine protein phosphatases at the dawn of a clinical era? Honkanen, R.E., Golden, T. Current medicinal chemistry. (2002) [Pubmed]
  21. Positive regulation of IkappaB kinase signaling by protein serine/threonine phosphatase 2A. Kray, A.E., Carter, R.S., Pennington, K.N., Gomez, R.J., Sanders, L.E., Llanes, J.M., Khan, W.N., Ballard, D.W., Wadzinski, B.E. J. Biol. Chem. (2005) [Pubmed]
  22. Protein phosphatase 2A-mediated cross-talk between p38 MAPK and ERK in apoptosis of cardiac myocytes. Liu, Q., Hofmann, P.A. Am. J. Physiol. Heart Circ. Physiol. (2004) [Pubmed]
  23. CRHSP-24 phosphorylation is regulated by multiple signaling pathways in pancreatic acinar cells. Schäfer, C., Steffen, H., Krzykowski, K.J., Göke, B., Groblewski, G.E. Am. J. Physiol. Gastrointest. Liver Physiol. (2003) [Pubmed]
  24. Okadaic acid overcomes the blocked cell cycle caused by depleting Cdc2-related kinases in Trypanosoma brucei. Li, Z., Tu, X., Wang, C.C. Exp. Cell Res. (2006) [Pubmed]
  25. Topoisomerase II inhibitors affect entry into mitosis and chromosome condensation in BHK cells. Anderson, H., Roberge, M. Cell Growth Differ. (1996) [Pubmed]
  26. Fostriecin: chemistry and biology. Lewy, D.S., Gauss, C.M., Soenen, D.R., Boger, D.L. Current medicinal chemistry. (2002) [Pubmed]
  27. Inhibition of type II topoisomerase by fostriecin. Boritzki, T.J., Wolfard, T.S., Besserer, J.A., Jackson, R.C., Fry, D.W. Biochem. Pharmacol. (1988) [Pubmed]
  28. Determination of fostriecin pharmacokinetics in plasma using high-pressure liquid chromatography assay. Pillon, L., Moore, M.J., Thiessen, J.J. Therapeutic drug monitoring. (1994) [Pubmed]
 
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