E-cadherin mediates contact inhibition of proliferation through Hippo signaling-pathway components

By Nam‐Gyun Kim, Eun-hie Koh, Xiao Chen, B. Gumbiner. Proceedings of the National Academy of Sciences of the United States of America, 2011

712 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/dedc71603ca2b259e797bc73ac14a60626046845

How researchers see this paper

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

In Cell Biology

1. K. Guan
2. S. Piccolo
3. Fa-Xing Yu
4. Bin Zhao
5. M. Cordenonsi
6. S. Dupont
7. Z. Meng
8. Duojia Pan

In Molecular Biology

1. K. Guan
2. Bin Zhao
3. S. Piccolo
4. Fa-Xing Yu
5. M. Cordenonsi
6. Duojia Pan
7. Z. Meng
8. S. Dupont

Citations in the corpus

• The biology of YAP/TAZ: hippo signaling and beyond. (2014, background): “(102) proposed that LATS is activated donwstream of E-cadherin-mediated adhesion, while Schlegelmilch et al.”
• VE-cadherin and endothelial adherens junctions: active guardians of vascular integrity. (2013, background): “The mechanism through which the cadherin complex restrains YAP signaling remains poorly understood, although a-catenin appears to be indirectly or directly implicated (Kim et al., 2011; Schlegelmilch et al., 2011; Silvis et al., 2011).”
• YAP/TAZ at the roots of cancer (2016, background): “, 2007); in these conditions, LATS1/2 inactivation increases nuclear YAP/TAZ levels, and LATS1/2 knockdown rescues cadherin-induced proliferative decline (Kim et al., 2011).”
• A mechanical checkpoint controls multicellular growth through YAP/TAZ regulation by actin-processing factors. (2013, neutral): “In this perspective, CIP would represent the response to a mechanical constraint: as cell crowding progressively boxes individual cells into smaller areas, these would be subjected to the same YAP/ TAZ-regulating mechanotransduction pathways that affect isolated cells plated on small ECM islands.”
• The two faces of Hippo: targeting the Hippo pathway for regenerative medicine and cancer treatment (2013, neutral): “Engagement of E-Cadherin (E-Cad) at adherens junctions suppresses YAP nuclear localization and activity through regulating MST activity 105 .”
• The Hippo pathway: regulators and regulations. (2013, background): “In mammalian cells, cell adhesion mediated by homophilic binding of E-cadherin led to YAP inactivation (Kim et al. 2011).”
• The E-Cadherin and N-Cadherin Switch in Epithelial-to-Mesenchymal Transition: Signaling, Therapeutic Implications, and Challenges (2019, background): “This showed that the cadherin-catenin complex, but not E-cadherin itself, was responsible for the regulation of Hippo-YAP1 signaling [155].”
• Mechanisms of Hippo pathway regulation (2016, neutral): “…of Msn, Hppy, and their mammalian homologs, MAP4Ks, have greatly broadened the scope of the Hippo pathway and also revealed the molecular basis of how various signals can activate LATS in MST1/2 knockout cells (Kim et al. 2011; Yu et al. 2012, 2013; Zhao et al. 2012; Meng et al. 2015).”
• Cell detachment activates the Hippo pathway via cytoskeleton reorganization to induce anoikis. (2012, background): “Several recent studies provided evidence that disruption of the E-cadherin–catenin complex at the cell–cell junction also leads to activation of YAP (Kim et al. 2011; Schlegelmilch et al. 2011; Silvis et al. 2011).”
• E-cadherin–integrin crosstalk in cancer invasion and metastasis (2013, background): “well as the Hippo signalling pathway (Kim et al., 2011).”
• The Hippo signaling pathway in stem cell biology and cancer (2014, neutral): “In addition, a multitude of other cellular junction proteins, such as PATJ, PALS1, AMOT (angiomotin), ZO-1 (zona occludens protein 1) [38,39], E-cadherin [40], a / b -catenin [41,42], PTPN14 (protein tyrosine phosphatase non-receptor type 14) [43 – 45], and Ajuba/Zyxin protein [46,47], have also bee”
• The Hippo pathway target, YAP, promotes metastasis through its TEAD-interaction domain (2012, background): “Although the membrane-proximal components of the mammalian Hippo pathway have not been elucidated fully, it is clear that the pathway is regulated by cell density (1, 2) as well as by changes in cell shape and in the actin cytoskeleton (3–5).”
• The Hippo Pathway: Biology and Pathophysiology. (2019, background): “The second potential mechanism is that trans-dimerization of E-cadherin at adherens junctions (AJs) stimulates the Hippo kinase cascade MST1/2-LATS1/2 through α/βcatenin, Kibra, and Merlin (Mer) (63).”
• The Hippo Signaling Pathway in Development and Disease (2019, background): “Besides the MAP4K subfamily, TAOK1 and TAOK3 were also reported to phosphorylate the HM of LATS1/2 in mammalian cells (Plouffe et al., 2016), although this activity is unlikely conserved for their Drosophila counterpart Tao-1 (Boggiano et al., 2011; Poon et al., 2011).”