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by Matsunaga, H. et al.
Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan

The Cu2+-induced potentiation of this interaction was abolished by amlexanox, which inhibits non-classical release of FGF1.
Neurochem. Int. 2008; 6:1076-85

[See paper]