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^[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).
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].

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

• . Camoni L, et al. The phytotoxin fusicoccin, a selective stabilizer of 14-3-3 interactions?. IUBMB Life. 2013;65(6):513-517.  [Content Brief]

  . Doveston RG, et al. Small-molecule stabilization of the p53-14-3-3 protein-protein interaction. FEBS Lett. 2017;591(16):2449-2457.  [Content Brief]

  . Kaplan A, et al. Small-Molecule Stabilization of 14-3-3 Protein-Protein Interactions Stimulates Axon Regeneration. Neuron. 2017;93(5):1082-1093.e5.  [Content Brief]

  [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.  [Content Brief]