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Review
, 1 (5), e26845

JNK Is a Novel Regulator of Intercellular Adhesion

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Review

JNK Is a Novel Regulator of Intercellular Adhesion

Hui You et al. Tissue Barriers.

Abstract

c-Jun N-terminal Kinase (JNK) is a family of protein kinases, which are activated by stress stimuli such as inflammation, heat stress and osmotic stress, and regulate diverse cellular processes including proliferation, survival and apoptosis. In this review, we focus on a recently discovered function of JNK as a regulator of intercellular adhesion. We summarize the existing knowledge regarding the role of JNK during the formation of cell-cell junctions. The potential mechanisms and implications for processes requiring dynamic formation and dissolution of cell-cell junctions including wound healing, migration, cancer metastasis and stem cell differentiation are also discussed.

Keywords: JNK; adherens junction; cell-cell adhesion; intercellular signaling; substrate stiffness.

Figures

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Figure 1. Schematic summarizing our recent findings. JNK binds to the adherens junction complex and phosphorylates β-catenin, preventing adherens junction formation. Upon inhibition of JNK kinase activity, β-catenin is dephosphorylated and adherens junctions are formed. Also α-catenin leaves the adherens junction complex and binds to actin, which is reorganized into parallel bundles underneath the adherens junction.,This figure was taken from Lee et alwith permission from the FASEB Journal.
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Figure 2. Schematic illustration of JNK regulating rigidity-dependent balance between focal adhesion (integrins) and cell-cell junction (cadherins).
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Figure 3. Analysis of tissue microarray data to uncover the correlation between p-JNK and E-cadherin levels in tumor cells. Tissues sections were graded on a 4-point scale based on the intensity of staining (from low to high 0, +1, +2, +3). The number of cells in each grade was counted using ImageJ.

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