For research use only. Not for therapeutic Use.
Fusicoccin (Fusicoccin A), a fungal pytotoxin, is a stabilizer of specific 14-3-3 protein-protein interactions. Fusicoccin sabilizes H+-ATPase/14-3-3 cmplex in pants, maintaining the enzyme in activated state. Fusicoccin also stabilizes 14-3-3 protein interactions with binding partners containing a C-terminal 14-3-3 recognition motif (a mode 3 motif), such as ERα, GPIbα, TASK3, CTFR, and p53. Fusicoccin induces apoptosis in cancer cells and has anticancer activity[1][2][3][4].
Fusicoccin (Fusicoccin A) stabilizes a complex between 14-3-3 and the stress response regulator GCN1, inducing GCN1 turnover and neurite outgrowth (EC50=29 mM)[3].
Fusicoccin A activates the plasma membrane H+-ATPase by stabilizing its binding to 14-3-3 proteins, which results in water loss and the wilting of infected plants. Fusicoccin A decreases the proliferation and migration of human GBM cell lines in vitro, including several cell lines that exhibit varying degrees of resistance to pro-apoptotic stimuli. The IC50 growth inhibitory concentration of fusicoccin A is 92 µM in the U373-MG cells and 83 µM in the Hs683 glioma cells[4].
Catalog Number | I014998 |
CAS Number | 20108-30-9 |
Synonyms | [(2S)-2-[(1E,3R,4S,8R,9R,10R,11S,14S)-8-[(2S,3R,4S,5R,6R)-4-acetyloxy-3,5-dihydroxy-6-(2-methylbut-3-en-2-yloxymethyl)oxan-2-yl]oxy-4,9-dihydroxy-14-(methoxymethyl)-3,10-dimethyl-6-tricyclo[9.3.0.03,7]tetradeca-1,6-dienyl]propyl] acetate |
Molecular Formula | C36H56O12 |
Purity | ≥95% |
InChI | InChI=1S/C36H56O12/c1-10-35(6,7)45-17-26-30(41)33(46-21(5)38)31(42)34(47-26)48-32-28-24(18(2)15-44-20(4)37)13-27(39)36(28,8)14-25-22(16-43-9)11-12-23(25)19(3)29(32)40/h10,14,18-19,22-23,26-27,29-34,39-42H,1,11-13,15-17H2,2-9H3/b25-14-/t18-,19-,22-,23+,26-,27+,29-,30-,31-,32-,33+,34-,36+/m1/s1 |
InChIKey | KXTYBXCEQOANSX-WYKQKOHHSA-N |
SMILES | CC1C2CCC(C2=CC3(C(CC(=C3C(C1O)OC4C(C(C(C(O4)COC(C)(C)C=C)O)OC(=O)C)O)C(C)COC(=O)C)O)C)COC |
Reference | [1]. Camoni L, et al. The phytotoxin fusicoccin, a selective stabilizer of 14-3-3 interactions?. IUBMB Life. 2013;65(6):513-517. [2]. Doveston RG, et al. Small-molecule stabilization of the p53-14-3-3 protein-protein interaction. FEBS Lett. 2017;591(16):2449-2457. [3]. Kaplan A, et al. Small-Molecule Stabilization of 14-3-3 Protein-Protein Interactions Stimulates Axon Regeneration. Neuron. 2017;93(5):1082-1093.e5. [4]. Bury M, et al. Fusicoccin a, a phytotoxic carbotricyclic diterpene glucoside of fungal origin, reduces proliferation and invasion of glioblastoma cells by targeting multiple tyrosine kinases. Transl Oncol. 2013;6(2):112-123. |