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Adaptor protein (AP) complexes play central roles in intracellular vesicular trafficking by coupling cargo selection to vesicle formation. AP-4, an important member of the AP family, plays a key role in this process. AP-4 dysfunction disrupts the transport of essential cargo proteins, such as ATG9A, leading to their abnormal retention within cells. However, the mechanistic details of how AP-4 is recruited to membranes and how its structural features support this process have remained unclear.

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