Trafficking protein particle complex subunit 9 (TRAPPC9)

Trafficking protein particle complex subunit 9 (TRAPPC9) is a key subunit of the TRAPPII complex involved in intracellular vesicle trafficking, primarily mediating transport from the endoplasmic reticulum (ER) to the Golgi apparatus, as well as intra-Golgi and endosome-to-Golgi transport[3][2][1]. It contains both TPR and ASH domains important for protein-protein and microtubule interactions[2]. TRAPPC9 is highly expressed in postmitotic neurons of the cerebral cortex and has a crucial role in neuronal development, synaptic plasticity, and neurogenesis[1]. It activates the NF-κB pathway by interacting with NIK and IKK-beta, linking vesicular transport with cell signaling[1][3][5]. Mutations in TRAPPC9 cause an autosomal-recessive form of intellectual disability often accompanied by developmental delay, obesity, and in some cases autism spectrum disorder and brain malformations[1][3][7][4]. While associated with cancer and liver diseases, it is not a current direct drug target; mutations primarily serve as genetic biomarkers for certain neurodevelopmental syndromes.

Other names

TRAPPC9NIBP (NIK- and IKK-beta-binding protein)T1IKBKBBPKIAA1882TRS120MRT13IBP

None established; no drugs are currently known to target TRAPPC9 directly for therapeutic purposes.