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. Author manuscript; available in PMC: 2007 Oct 1.
Published in final edited form as: Gastroenterology. 2006 Aug 22;131(4):1153–1163. doi: 10.1053/j.gastro.2006.08.022

Figure 10.

Figure 10.

TNFR2-dependent tight junction disruption is accompanied by increases in MLC phosphorylation and MLCK expression.

IFN-γ-primed non-transfected monolayers and TNFR2-transfected monolayers were harvested 8 hours after treatment with 2.5 ng/ml TNF, as indicated. SDS-PAGE and immunoblot shows 2.8±0.4-fold and 2.9±0.1-fold induction of MLCK expression after TNF treatment of IFN-γ-primed non-transfected monolayers and TNFR2-transfected monolayers, respectively (p<0.02 for both). MLC phosphorylation increased 2.0±0.1-fold and 1.9±0.2-fold after TNF treatment of IFN-γ-primed non-transfected monolayers and TNFR2-transfected monolayers, respectively (p<0.01 for both). Total MLC is shown as a loading control. Data are representative of 3 independent experiments, each with triplicate samples.