{"id":20,"date":"2026-07-01T08:13:33","date_gmt":"2026-07-01T08:13:33","guid":{"rendered":"https:\/\/cellbiology-dev.i-med.ac.at\/?page_id=20"},"modified":"2026-07-20T09:07:09","modified_gmt":"2026-07-20T09:07:09","slug":"the-vogel-laboratory","status":"publish","type":"page","link":"https:\/\/cellbiology-dev.i-med.ac.at\/index.php\/the-vogel-laboratory\/","title":{"rendered":"The Vogel Laboratory"},"content":{"rendered":"\n

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The Vogel Laboratory: Intracellular Cargo Transport in Congenital Intestinal Diseases<\/h1>\n\n\n\n

We are focusing on congenital intestinal and liver diseases, which are often caused by mutations in genes that are essential for correct intestinal-epithelial polarization. For example, we have identified mutations in MYO5B and STX3 in microvillus inclusion disease: both genes are essential for the polarized apical cargo transport of transmembrane transporters (Vogel GF et al., JCB, 2015; Vogel GF et al., JCI Insight, 2017; Szab\u00f3 L et al., Traffic, 2024). We are now turning our attention to myo5b-associated cholestatic liver disease and myo5b-independent apical transport in intestinal epithelial cells.<\/p>\n\n\n\n

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Schematic representation of a healthy polarized intestinal epithelial cell (A), with proteins relevant for intracellular polarized trafficking and apical digestive\/resorptive function highlighted (B), and trafficking and polarity defects depicted upon mutations in MYO5B<\/em>, STX3<\/em>, STXBP2<\/em> or UNC45-A <\/em>(taken from Szab\u00f3 L et al., Traffic, 2024).<\/em><\/figcaption><\/figure>\n\n\n\n

Moreover, we are interested in describing novel genetic variants associated with congenital enteropathies or hepatopathies. We recently described the first case of a congenital enteropathy due to mutations in ezrin (Vogel GF et al., Human Genetics, 2025), a protein involved in the establishment of proper apical polarity and plasma membrane composition in epithelial cells, as well as the first cases of acute liver failure associated with variants in the TRPM7<\/em> gene (Schlieben LD et al., Hepatology Communications 2024).<\/p>\n\n\n\n

We are also addressing the role of the retriever complex and the poorly characterized protein TM9SF4 in polarized plasma membrane cargo trafficking in epithelial cells.<\/p>\n\n\n\n

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Schematic representation of hepatocytes with various subcellular compartments shown (A), and highlighted proteins associated with trafficking defects in congenital liver disease (B).<\/figcaption><\/figure>\n\n\n\n

Furthermore, we study the liver immunesystem associated with acute hepatitis of unknown origin (R\u00f6ttele F et al., Gut 2025) and autoimmune liver disease, the enterohepatic circulation in patients with progressive familial intrahepatic cholestasis (PFIC1), and the role of the gut microbiome in association with gut and hepatic diseases (Z\u00f6ggeler T et al., Gut Microbes 2025; Aldrian D et al., Inflammatory Bowel Diseases 2025).<\/p>\n\n\n\n

Publications<\/h2>\n\n\n\n