Marchiando, Amanda M., Shen, Le, Graham, W. Vallen, Weber, Christopher R., Schwarz, Brad T., Austin, Jotham R., Raleigh, David R., Guan, Yanfang, Watson, Alastair J. M. ORCID: https://orcid.org/0000-0003-3326-0426, Montrose, Marshall H. and Turner, Jerrold R. (2010) Caveolin-1-dependent occludin endocytosis is required for TNF-induced tight junction regulation in vivo. Journal of Cell Biology, 189 (1). pp. 111-126. ISSN 0021-9525
Full text not available from this repository.Abstract
Epithelial paracellular barrier function, determined primarily by tight junction permeability, is frequently disrupted in disease. In the intestine, barrier loss can be mediated by tumor necrosis factor (alpha) (TNF) signaling and epithelial myosin light chain kinase (MLCK) activation. However, TNF induces only limited alteration of tight junction morphology, and the events that couple structural reorganization to barrier regulation have not been defined. We have used in vivo imaging and transgenic mice expressing fluorescent-tagged occludin and ZO-1 fusion proteins to link occludin endocytosis to TNF-induced tight junction regulation. This endocytosis requires caveolin-1 and is essential for structural and functional tight junction regulation. These data demonstrate that MLCK activation triggers caveolin-1-dependent endocytosis of occludin to effect structural and functional tight junction regulation.
Item Type: | Article |
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Uncontrolled Keywords: | animals,caveolin 1,endocytosis,membrane proteins,mice,mice, transgenic,occludin,phosphoproteins,signal transduction,tight junctions,tumor necrosis factor-alpha,zonula occludens-1 protein |
Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
UEA Research Groups: | Faculty of Medicine and Health Sciences > Research Groups > Gastroenterology and Gut Biology |
Depositing User: | EPrints Services |
Date Deposited: | 25 Nov 2010 11:13 |
Last Modified: | 20 Aug 2023 00:09 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/15144 |
DOI: | 10.1083/jcb.200902153 |
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