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

Ponasterone A     (2S,3R,5R,10R,13R,14S,17S)- 17-[(3R)-2,3...

Synonyms:
 
 
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Disease relevance of Ponasterone A

 

High impact information on Ponasterone A

  • Ponasterone A is a potent regulator of gene expression in cells and transgenic animals, enabling reporter genes to be turned on and off rapidly [5].
  • To address the physiologic significance of 53BP2 induction, we utilized stable cell lines with a ponasterone A-regulated 53BP2 cDNA [6].
  • In contrast, in vitro-transcribed-translated USP-1 and USP-2 both formed heterodimeric complexes with EcR-B1 that bound ponasterone A with the same Kd (7 x 10(-10) M) and bound to both EcRE1 and heat shock protein 27 EcRE [7].
  • To additionally understand the significance of the MAD2 to mitotic checkpoint control, we established an inducible expression system in which MAD2 was induced by the addition of ponasterone A [8].
  • Pharmacokinetic analysis of a highly bioactive ligand (ponasterone A), identified through screening ecdysteroids from local plants, demonstrated sustained release and transgene expression in vivo [9].
 

Biological context of Ponasterone A

  • In current studies, the nature of the heterodimers was investigated by producing the phenotypes of the 1:1 heterodimers formed between the constitutively expressed mu-opioid receptor (MOR) and the ponasterone A-induced expression of delta-opioid receptor (DOR) in EcR293 cells [10].
  • The crystal structures of the ligand-binding domains (LBDs) of the EcR/USP heterodimer, complexed to the ecdysteroid ponasterone A (ponA) and to the lepidopteran specific bisacylhydrazine BYI06830 used in the agrochemical pest control, provide the first insight at atomic level for these important functional complexes [11].
  • Both wild type and T187A mutant protein induced by 5 microM ponasterone A inhibited cell growth and increased cell number at the G1 phase [12].
  • Stereoselective synthesis of (22R)- and (22S)-castasterone/ponasterone A hybrid compounds and evaluation of their molting hormone activity [13].
  • After incubation of intact Kc cells, 200-300 specific binding sites were detected for both 20-OH ecdysone and ponasterone A [14].
 

Anatomical context of Ponasterone A

 

Associations of Ponasterone A with other chemical compounds

 

Gene context of Ponasterone A

  • Treatment of cells with the synthetic ecdysone analog ponasterone A induced expression of GFP-MKK7(3E) and resulted in sustained activation of endogenous JNK, but neither of the other endogenous MAPKs, ERK or p38 [23].
  • Expression of both ABCA1 and ABCA7 was induced linearly proportional to ponasterone A concentration in the medium [24].
  • Induction of cyclin D1 antisense mRNA by the ecdysteroid, ponasterone A, resulted in a 55% decrease in cyclin D1 mRNA and a 58% decrease in CD1 protein levels [25].
  • The BACE1 protein level was increased in a time- and dosage-dependent manner in the inducible BACE1 stable cells by treatment with inducer ponasterone A [26].
  • USP and EcR fusion proteins could be expressed in separate cell lines and then recombined following isolation to yield a ligand binding preparation with a dissociation constant (K(D)) for Ponasterone A of 1.5 nM and a total yield of 1.9 pmol ligand binding sites/mg protein [27].
 

Analytical, diagnostic and therapeutic context of Ponasterone A

  • RESULTS: After treatment with ponasterone A, we could find an induction of both p27(Kip1) wild type and T187A mutant protein [12].
  • Using cDNA arrays and quantitative PCR, we discovered nine genes whose expression was increased, but no genes whose expression was reduced, following 24 h of induction with Ponasterone A (PonA), a ligand for EcR [28].
  • However, other minor compounds have been detected (some unknown, others migrating like ecdysone and ponasterone A in HPLC) [29].
  • Following the onset of feeding, there appeared both specific ponasterone A binding and two major EcR bands detected by Western blot analysis [30].
  • DU145 cell cultures in complete medium exhibited a maximum of approximately 28% of apoptotic cells after 96 h of exposure to an ecdysone analog, Ponasterone A [31].

References

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  10. Heterodimerization of mu- and delta-opioid receptors occurs at the cell surface only and requires receptor-G protein interactions. Law, P.Y., Erickson-Herbrandson, L.J., Zha, Q.Q., Solberg, J., Chu, J., Sarre, A., Loh, H.H. J. Biol. Chem. (2005) [Pubmed]
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  12. Transfection of p27(Kip1) threonine residue 187 mutant type gene, which is not influenced by ubiquitin-mediated degradation, induces cell cycle arrest in oral squamous cell carcinoma cells. Kudo, Y., Kitajima, S., Sato, S., Ogawa, I., Miyauchi, M., Takata, T. Oncology (2002) [Pubmed]
  13. Stereoselective synthesis of (22R)- and (22S)-castasterone/ponasterone A hybrid compounds and evaluation of their molting hormone activity. Watanabe, B., Nakagawa, Y., Ogura, T., Miyagawa, H. Steroids (2004) [Pubmed]
  14. A reappraisal of ecdysteroid binding in Drosophila. Gronemeyer, H., Harry, P., Alberga, A. Mol. Cell. Endocrinol. (1983) [Pubmed]
  15. Development of a ponasterone A-inducible gene expression system for application in cultured skeletal muscle cells. Xiao, Y.Y., Beilstein, M.A., Wang, M.C., Purintrapiban, J., Forsberg, N.E. Int. J. Biochem. Cell Biol. (2003) [Pubmed]
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  19. Studies on the biosynthesis of ecdysone by the Y-organs of Carcinus maenas. Lachaise, F., Meister, M.F., Hétru, C., Lafont, R. Mol. Cell. Endocrinol. (1986) [Pubmed]
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  21. The ecdysone inducible gene expression system: unexpected effects of muristerone A and ponasterone A on cytokine signaling in mammalian cells. Constantino, S., Santos, R., Gisselbrecht, S., Gouilleux, F. Eur. Cytokine Netw. (2001) [Pubmed]
  22. Structural adaptability in the ligand-binding pocket of the ecdysone hormone receptor. Billas, I.M., Iwema, T., Garnier, J.M., Mitschler, A., Rochel, N., Moras, D. Nature (2003) [Pubmed]
  23. Inducible expression of a constitutively active mutant of mitogen-activated protein kinase kinase 7 specifically activates c-JUN NH2-terminal protein kinase, alters expression of at least nine genes, and inhibits cell proliferation. Wolter, S., Mushinski, J.F., Saboori, A.M., Resch, K., Kracht, M. J. Biol. Chem. (2002) [Pubmed]
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