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and QA impaired cognition and neurite structure via NMDAR-mediated reductions in brain-derived neurotrophic factor (BDNF), an effect that was blocked by an NMDAR antagonist [91]

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Furthermore, several inhibitors (e.g., DC-TEADin02 and K-975) that target the autopalmitoylation pocket of the TEA domain (TEAD) of transcription factors occupy this hydrophobic cavity, where they competitively inhibit TEAD autopalmitoylation and consequently disrupt its oncogenic transcriptional activity [187, 188]

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