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Point mutations in Arf1 reveal cooperative effects of the N-terminal extension and myristate for GTPase-activating protein catalytic activity

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under normal conditions, BDNF binds to TrkB receptors to activate pathways such as ERK and Akt, activating the mammalian target of rapamycin complex 1 (mTORC1), which drives synaptic protein synthesis, promoting dendritic spine and synapse formation, and maintaining synaptic structures (118)