Soluble E-cadherin promotes cell survival by activating epidermal growth factor receptor (Q83143406)

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19 January 2020

title

Soluble E-cadherin promotes cell survival by activating epidermal growth factor receptor (English)

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19 January 2020

Sonali P. Barwe

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21 November 2024

Julia D'Ambrosio

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19 January 2020

Jegan Gopal

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19 January 2020

Kan Lu

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19 January 2020

Sergey Ryazantsev

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19 January 2020

Landon J. Inge

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21 November 2024

Sigrid A. Rajasekaran

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21 November 2024

Ayyappan K. Rajasekaran

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21 November 2024

language of work or name

English

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publication date

4 January 2011

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full work available at URL

19 January 2020

https://api.elsevier.com/content/article/PII:S0014482710005835?httpAccept=text/xml

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Crossref

DOI

https://api.crossref.org/works/10.1016/J.YEXCR.2010.12.025

https://api.elsevier.com/content/article/PII:S0014482710005835?httpAccept=text/plain

21 November 2024

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Crossref

DOI

https://api.crossref.org/works/10.1016/J.YEXCR.2010.12.025

Experimental Cell Research

21 November 2024

published in

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19 January 2020

volume

317

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19 January 2020

issue

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19 January 2020

page(s)

838-848

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Cell adhesion and signalling by cadherins and Ig-CAMs in cancer

19 January 2020

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E-cadherin homophilic ligation directly signals through Rac and phosphatidylinositol 3-kinase to regulate adhesive contacts

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Signaling from E-cadherins to the MAPK pathway by the recruitment and activation of epidermal growth factor receptors upon cell-cell contact formation.

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Enhanced activation of epidermal growth factor receptor caused by tumor-derived E-cadherin mutations

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Autoregulation of E-cadherin expression by cadherin-cadherin interactions: the roles of beta-catenin signaling, Slug, and MAPK

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Motility enhancement by tumor-derived mutant E-cadherin is sensitive to treatment with epidermal growth factor receptor and phosphatidylinositol 3-kinase inhibitors

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Down-regulation of E-cadherin in human bronchial epithelial cells leads to epidermal growth factor receptor-dependent Th2 cell-promoting activity.

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Activation of the protein kinase Akt/PKB by the formation of E-cadherin-mediated cell-cell junctions. Evidence for the association of phosphatidylinositol 3-kinase with the E-cadherin adhesion complex.

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Formation of E-cadherin-mediated cell-cell adhesion activates AKT and mitogen activated protein kinase via phosphatidylinositol 3 kinase and ligand-independent activation of epidermal growth factor receptor in ovarian cancer cells

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Early loss of E-cadherin from cell-cell contacts is involved in the onset of Anoikis in enterocytes

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E-cadherin cell-cell adhesion in ewing tumor cells mediates suppression of anoikis through activation of the ErbB4 tyrosine kinase

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Truncated E-cadherin potentiates cell death in prostate epithelial cells

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The ectodomain shedding of E-cadherin by ADAM15 supports ErbB receptor activation

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Serum-soluble E-cadherin fragments in lung cancer

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Cell adhesion molecules in bladder cancer: soluble serum E-cadherin correlates with predictors of recurrence

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Soluble E-cadherin fragments increased in circulation of cancer patients

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Urinary concentrations of the soluble adhesion molecule E-cadherin and total protein in patients with bladder cancer

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Engagement of collagen-binding integrins promotes matrix metalloproteinase-9-dependent E-cadherin ectodomain shedding in ovarian carcinoma cells

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Soluble E-cadherin is an independent pretherapeutic factor for long-term survival in gastric cancer

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19 January 2020

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