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Vesicle transport protein GOT1B (GOLT1B) is a highly conserved tetra-spanning membrane protein encoded by the *GOLT1B* gene in humans, primarily localized to the Golgi apparatus[1][2]. It plays a central role in vesicle-mediated transport between the endoplasmic reticulum (ER) and Golgi, as well as in endosome-Golgi traffic, working in concert with related proteins like Sf2p[1][2]. Experimental studies show that loss of GOLT1B disrupts ER-Golgi trafficking, affecting vesicle tethering, Golgi ion homeostasis, and potentially calcium release[1][2]. GOLT1B is overexpressed in many cancer types and its amplification is consistently correlated with poor prognosis and metastasis, particularly via the induction of epithelial-mesenchymal transition (EMT) and modulation of immune checkpoints such as PD-L2[4][5]. Functional studies in colorectal cancer models support its emerging role as an oncogenic driver and prognostic biomarker, and as a promising target for RNA interference therapeutics, although no direct small-molecule or antibody drugs have been described to date[4][5].
Not applicable for marketed drugs (no direct drug targeting reported) siRNA-directed knockdown leads to inhibition of cancer growth/metastasis in models[5]
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