Cadherins and catenins in development
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Cited by (308)
sFRP4 signalling of apoptosis and angiostasis uses nitric oxide-cGMP-permeability axis of endothelium
2017, Nitric Oxide - Biology and ChemistryCitation Excerpt :An intact endothelial monolayer demonstrates low-level “basal” permeability. Acute and short-term hyperpermeability, induced by vascular permeability factors such as VPF/VEGF-A and other vascular permeabilizing agents, define pro-angiogenic events by cross talking with small GTPases, cytokines and adherence junctions [22]. However in regards to the mechanism underlying the anti-angiogenic role of sFRP4, our previous studies were only able to hint that the anti-angiogenesis effect was mediated indirectly as a consequence sFRP4 suppression of nuclear translocation of β-catenin and elevated intracellular reactive oxygen species (ROS) induced apoptotic death.
Overexpression of signal transducers and activators of transcription in embryos derived from vitrified oocytes negatively affect E-cadherin expression and embryo development
2015, CryobiologyCitation Excerpt :Besides IL-6-family of cytokines (IL-6, CNTF, OSM and LIF), and the growth factors EGF and PDGF, the Src-family of tyrosine kinases [6] and leptin can phosphorylate and activate STAT3 in mammalian cells. After phosphorylation, Stat proteins can form dimers, translocate into the nucleus and activate gene expression by binding to specific response elements in the promoter of target genes [22]. There are also evidences indicating the bidirectional relationship between CDH1 and STAT3 in mammalian cells [18,19].
β-Catenin serves as a clutch between low and high intercellular E-cadherin bond strengths
2013, Biophysical Journal