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results reveal that miR-130a directly targets FOSL1 and suppresses the inhibition of ZO-1, thus inhibiting cancer cell migration and invasion, in triple-negative breast cancer.
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Study findings show for the first time that the systemic concentration of ZO-1 was significantly elevated in Hepatocellular carcinoma (HCC) patients and is positively correlated with inflammatory markers and raise the possibility that it could be used as a potential diagnostic biomarker for HCC progression.
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Dysfunction of the miR-455-TJP1 axis is involved in bladder cancer cell growth and metastasis.
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The tight junction protein ZO-1 exists in stretched and folded conformations within epithelial cells, depending on actomyosin-generated force.
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miR103 was upregulated in CRC. Overexpression of miR103 promoted CRC cell proliferation and migration in vitro, whereas downregulation of miR103 inhibited cell proliferation and migration. ZO1 was identified as a direct target of miR103, revealing its expression to be inversely correlated with miR103 expression in CRC samples.
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SHANK3 expression correlated with ZO-1 and PKCepsilon in colonic tissue of patients with Crohn's disease. The expression level of SHANK3 affects ZO-1 expression and the barrier function in intestinal epithelial cells.
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These results indicate the varying effects of 7-oxygenated cholesterol molecules on the expression and localization of ZO-1 depending on cell types, and suggest the contribution of 7-oxygeneted cholesterol molecules to the structural alteration of tight junctions.
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CTR activates AKAP2-anchored cAMP-dependent protein kinase A, which then phosphorylates tight junction proteins ZO-1 and claudin 3.
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the Ras signaling pathway is involved in HIV-1 Tat-induced changes in ZO-1 and NEP.
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decreased interaction between ZO-1 and occludin might contribute to the epiphora occurred in the transplanted submandibular glands
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integration of claudin-2, occludin and ZO-1 is necessary for maintaining the function of the proximal tubular epithelium.
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Endothelial cellsTLR4 strongly regulates retinal vessel permeability by reducing expression of occludin and zonula occludens 1.
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The role of estrogens in the regulation of ZO-1 and estrogen receptors 1 and 2 was evaluated in human primary gut tissues by immunohistochemistry, immunofluorescence and qPCR.
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Aberrant expression of the tight junction molecules claudin-1 and zonula occludens-1 mediates cell growth and invasion in oral squamous cell carcinoma cells.
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ZO-1-occludin interactions regulate multiple phases of epithelial polarization by providing cell-intrinsic signals that are required for single lumen formation.
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It is postulated that ZO-1, when not phosphorylated by PKC, keeps Octn2 in an active state, while elimination of this binding in DeltaPDZ mutant or after ZO-1 phosphorylation leads to diminution of Octn2 activity.
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Results uncovered ZO-1 as part of a signaling node activated by VEGF, but not Ang-1, that specifically modulates endothelial cells proliferation during angiogenesis.
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Data suggest that long noncoding RNA PlncRNA1 and microRNA miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin.
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STAT3 activation downregulates the ZO-1 and occludin levels and increases the endothelial permeability through the induction of VEGF production in retinal endothelial cells.
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Data show that tight junction protein 1 (TJP1) suppressed expression of the catalytically proteasome subunits LMP7 and LMP2, decreased proteasome activity, and enhanced proteasome inhibitor sensitivity in vitro and in vivo through suppression of EGFR/JAK1/STAT3 signaling.
