Reference : AMP-activated protein kinase (AMPK) activation and glycogen synthase kinase-3beta (GS...
Scientific journals : Article
Life sciences : Anatomy (cytology, histology, embryology...) & physiology
AMP-activated protein kinase (AMPK) activation and glycogen synthase kinase-3beta (GSK-3beta) inhibition induce Ca2+-independent deposition of tight junction components at the plasma membrane.
Zhang, Lihong [Université de Liège - ULiège > Département Argenco : Secteur MS2F > Adéquat. struct. aux exig. de fonct.& perfor. techn.-écon. >]
JOURET, François mailto [Centre Hospitalier Universitaire de Liège - CHU > > Néphrologie >]
Rinehart, Jesse [> >]
Sfakianos, Jeff [> >]
Mellman, Ira [> >]
Lifton, Richard P. [> >]
Young, Lawrence H. [> >]
Caplan, Michael J. [> >]
Journal of Biological Chemistry
Yes (verified by ORBi)
United States
[en] AMP-Activated Protein Kinases/metabolism/physiology ; Animals ; Cadherins/metabolism ; Calcium/metabolism ; Cell Adhesion ; Cell Membrane/metabolism ; Dogs ; Epithelium/metabolism ; Gene Expression Regulation, Enzymologic ; Glycogen Synthase Kinase 3/antagonists & inhibitors/physiology ; Membrane Proteins/antagonists & inhibitors/metabolism/physiology ; Microscopy, Fluorescence/methods ; Phosphoproteins/metabolism ; Phosphorylation ; RNA Interference ; Tight Junctions/metabolism
[en] Extracellular Ca(2+) is essential for the development of stable epithelial tight junctions. We find that in the absence of extracellular Ca(2+), AMP-activated protein kinase (AMPK) activation and glycogen synthase kinase (GSK)-3beta inhibition independently induce the localization of epithelial tight junction components to the plasma membrane. The Ca(2+)-independent deposition of junctional proteins induced by AMPK activation and GSK-3beta inhibition is independent of E-cadherin. Furthermore, the nectin-afadin system is required for the deposition of tight junction components induced by AMPK activation, but it is not required for that induced by GSK-3beta inhibition. Phosphorylation studies demonstrate that afadin is a substrate for AMPK. These data demonstrate that two kinases involved in regulating cell growth and metabolism act through distinct pathways to influence the deposition of the components of epithelial tight junctions.

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