Sticky business: orchestrating cellular signals at adherens junctions.

By Mirna Perez‐Moreno, C. Jamora, Elaine Fuchs. Cell, 2003

803 citations recorded by the source corpus.

Subfields: Immunology and Allergy, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3251e44d19cd8cc97c4cf991ba250b7e9562890e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology and Allergy

In Molecular Biology

Citations in the corpus

E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer (2009, background): “cytoskeleton, thereby mediating mechanical stability [15, 16].”
Epidermal stem cells of the skin. (2006, background): “…cells utilize a more dynamic cytoskeletal network of microtubules and actin filaments that interface through βand α-catenins to E-cadherin-mediated cellcell (adherens) junctions, in addition to the αβ1-integrin-mediated cell-ECM junctions (reviewed in Green et al. 2005, Perez-Moreno et al. 2003).”
TGF-β and epithelial-to-mesenchymal transitions (2005, background): “…of Par6 allows it to recruit Smurf1 which in turn leads to ubiquitination and degradation of RhoA (Ozdamar et al., 2005), a small GTPase family member responsible for stress fiber formation and for the maintenance of apico-basal polarity and junctional stability (Perez-Moreno et al., 2003).”
Intestinal barrier function: molecular regulation and disease pathogenesis. (2009, background): “Cadherin-catenin complexes are important not only for linking adjacent cells but also for maintaining cell polarity, regulating epithelial migration and proliferation, and forming other adhesive complexes, such as desmosomes.(19,21,27) In support of this, downregulation of E-cadherin in the intestin”
Cell adhesion and signalling by cadherins and Ig-CAMs in cancer (2004, background): “Phosphatidylinositol 3-kinase (PI3K) is recruited to the membrane by intact E-cadherin adhesion junctions, where it generates phosphatidylinositol-(3,4,5)triphosphate (PIP3), resulting in the activation of the RHO-GEF TIAM1 and subsequently of RAC1 and CDC42.”
Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis. (2006, background): “D formation of catenin-containing complexes that link E-cadherin to the actin and microtubule cytoskeleton (Hulsken et al., 1994; Takeichi, 1995; Perez-Moreno et al., 2003).”
Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “…adhesion and polarity in epithelia depends on the formation of adherens junctions in which E-cadherin is a key determinant, providing the physical structure for both cell–cell attachment and the recruitment of signalling complexes (reviewed by Knust and Bossinger, 2002; Perez-Moreno et al., 2003).”
E-cadherin mediates contact inhibition of proliferation through Hippo signaling-pathway components (2011, background): “Its adhesive function at the cell surface leads to a junctional barrier, limiting the accessibility of growth factors to their receptors, inhibition cell movement out of the epithelium, and the establishment of many cell–cell interactions that indirectly inhibit cell growth, including tight junction”
Socializing with the neighbors: stem cells and their niche. (2004, background): “…subsets of factors, dle oriented perpendicular to the interface of the hub cell and the GSC, with one of the spindle poles nestledincluding APC, dynein-dynactin, PKC , actin, and myo- sins (reviewed by Perez-Moreno et al., 2003; Petritsch into this crescent of heterotypic contact (Figure 4B).”