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Trafficking protein particle complex subunit 6A (TRAPPC6A)

Target
TRAPPC6A
Molecular classification
Other (vesicular trafficking machinery protein; subunit of multisubunit tethering complex)
01

Overview

Trafficking protein particle complex subunit 6A (TRAPPC6A) is a core component of the TRAPP (Trafficking Protein Particle) complexes, which mediate tethering of transport vesicles to the cis-Golgi membrane and regulate intracellular protein trafficking between the endoplasmic reticulum and Golgi apparatus[1][3]. TRAPPC6A acts primarily as a structural subunit, interacting with other components to stabilize the formation of higher-order TRAPP complexes (TRAPPII, TRAPPIII), critical for normal vesicular trafficking[1]. TRAPPC6A is a target for ubiquitination and normally degraded by the proteasome; mutations or aggregation of TRAPPC6A have been linked to neurological disorders such as intellectual disability as well as to neurodegenerative diseases like Alzheimer’s disease, where it has been found to aggregate and potentially drive Tau and amyloid pathology in conjunction with loss of WWOX[1][2]. Differential expression and dysfunction of TRAPPC6A have been associated with certain forms of heart failure, indicating a role in cardiovascular disease as well[1]. There are no known drugs that directly target TRAPPC6A, and it is not considered a canonical therapeutic target (such as a receptor, enzyme, or channel); its pathogenic and biomarker roles derive instead from its protein trafficking and aggregation properties.

Other names
TRAPPC6ATRS33Trafficking protein particle complex 6ATRAPPC6AΔTPC6AHSPC289MGC2650
02

Biological functions

Vesicle tethering to the cis-Golgi membraneProtein trafficking (between ER and Golgi)Stabilization of TRAPP complexes (TRAPPII, TRAPPIII)Ubiquitination substrate, proteasomal degradationPotential role in neuronal development
03

Disease associations

Neurodevelopmental disorders (intellectual disability, speech delay, polydactyly, facial dimorphism)Alzheimer’s disease (aggregation can trigger pathological cascades)Cardiovascular disease (associated with right ventricular heart failure expression changes)
04

Safety considerations

Protein aggregation associated with neurodegeneration (Alzheimer’s disease)Ubiquitin-proteasome system dysfunction can cause inappropriate protein accumulation
05

Biomarkers

TRAPPC6A aggregation (potential marker for Alzheimer’s disease progression)Differential TRAPPC6A mRNA/protein expression in heart failure (potential cardiovascular biomarker)

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