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Protein SEC13 homolog (**SEC13**) is a highly conserved, dual-function structural protein that serves as a core component of both the COPII coat complex—required for vesicle-mediated protein trafficking from the endoplasmic reticulum (ER) to the Golgi apparatus—and the nuclear pore complex (NPC), which facilitates nucleo-cytoplasmic transport[1][2][3][5]. SEC13 interacts with SEC31 to form the outer coat of COPII vesicles, essential for protein export from the ER. In the NPC, SEC13 is required for nuclear pore formation, regulating import and export between the nucleus and cytoplasm. SEC13 also functions as part of the GATOR2 complex, regulating mTORC1 signaling. Loss of SEC13 impairs both endomembrane and nuclear transport, leading to developmental defects (such as defective retinal lamination and digestive organ hypoplasia, via activation of p53-dependent apoptosis). Its essential structural and regulatory roles across multiple large protein complexes make SEC13 critical for cell viability and organismal development[1][2][4][5]. **NOTES:** - *SEC13 is not typically considered a direct therapeutic target (such as a receptor, enzyme, or transporter). There is no evidence for clinical-stage drugs or tool compounds targeting SEC13 directly or indirectly in humans.* - *SEC13 loss-of-function or mutation studies highlight its necessity for fundamental cell processes in both animals and humans, with tissue-specific phenotypes (e.g., retina, digestive organs) upon experimental inactivation[1][2][3].* - *No known FDA-approved or investigational drugs are reported to directly interact with or modulate SEC13.* - *SEC13's high essentiality and involvement in basic cellular machinery raise major safety concerns regarding systemic inhibition.*
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