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Publication : Caveolin-1-dependent occludin endocytosis is required for TNF-induced tight junction regulation in vivo.

First Author  Marchiando AM Year  2010
Journal  J Cell Biol Volume  189
Issue  1 Pages  111-26
PubMed ID  20351069 Mgi Jnum  J:158798
Mgi Id  MGI:4440663 Doi  10.1083/jcb.200902153
Citation  Marchiando AM, et al. (2010) Caveolin-1-dependent occludin endocytosis is required for TNF-induced tight junction regulation in vivo. J Cell Biol 189(1):111-26
abstractText  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.
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