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Synaptotagmin-17 (SYT17) is a member of the synaptotagmin family of membrane-trafficking proteins distinguished by the presence of C2 domains but lacks the ability to directly participate in exocytosis typical of classical synaptotagmins. SYT17 is highly expressed in neurons, especially in the hippocampus, where it localizes to both the Golgi complex and early endosomes. In the Golgi, SYT17 coordinates the import of vesicles from the endoplasmic reticulum, supporting neurite outgrowth and axon regeneration following neuronal injury. It also plays a critical role in early endosomes, regulating endocytic trafficking and controlling the postsynaptic accumulation of AMPA-type glutamate receptors, which is vital for maintaining synaptic plasticity and normal synaptic physiology. Loss of SYT17 disrupts these processes, leading to impaired axonal regrowth and defective synaptic signaling. SYT17 has been implicated in neurodevelopmental and neurodegenerative disorders due to its role in synaptic function and plasticity, and genetic variation in SYT17 is associated with risk for autism spectrum disorder. To date, there are no known drugs directly targeting SYT17, and it is not an established therapeutic target, but its unique functional roles make it of increasing research interest in neurobiology and neuroregeneration contexts.
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