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Galectin-4 andsulfatides in apicalmembrane traffickingin enterocyte-likecells Delphine DelacourValérie GouyerJean‐Pierre Zanetta2005 год

Galectin-4 and sulfatides in apical membrane trafficking in enterocyte-like cells
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Аннотация: We have previously reported that 1-benzyl-2-acetamido-2-deoxy-α-d-galactopyranoside (GalNAcα-O-bn), an inhibitor of glycosylation, perturbed apical biosynthetic trafficking in polarized HT-29 cells suggesting an involvement of a lectin-based mechanism. Here, we have identified galectin-4 as one of the major components of detergent-resistant membranes (DRMs) isolated from HT-29 5M12 cells. Galectin-4 was also found in post-Golgi carrier vesicles. The functional role of galectin-4 in polarized trafficking in HT-29 5M12 cells was studied by using a retrovirus-mediated RNA interference. In galectin-4–depleted HT-29 5M12 cells apical membrane markers accumulated intracellularly. In contrast, basolateral membrane markers were not affected. Moreover, galectin-4 depletion altered the DRM association characteristics of apical proteins. Sulfatides with long chain-hydroxylated fatty acids, which were also enriched in DRMs, were identified as high-affinity ligands for galectin-4. Together, our data propose that interaction between galectin-4 and sulfatides plays a functional role in the clustering of lipid rafts for apical delivery.
Год издания: 2005
Авторы: Delphine Delacour, Valérie Gouyer, Jean‐Pierre Zanetta, Hervé Drobecq, Emmanuelle Leteurtre, Georges Grard, Odile Moreau-Hannedouche, Emmanuel Maes, Alexandre Pons, Sabine André, André Le Bivic, Hans‐Joachim Gabius, Aki Manninen, Kai Simons, Guillemette Huet
Издательство: Rockefeller University Press
Источник: The Journal of Cell Biology
Ключевые слова: Galectins and Cancer Biology, Glycosylation and Glycoproteins Research, Toxin Mechanisms and Immunotoxins
Другие ссылки: The Journal of Cell Biology (PDF)
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HAL (Le Centre pour la Communication Scientifique Directe) (HTML)
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HAL (Le Centre pour la Communication Scientifique Directe) (HTML)
Europe PMC (PubMed Central) (PDF)
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PubMed Central (HTML)
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