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Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules
Published on: October 17, 2014
Soluble E-cadherin: more than a symptom of disease.
Magdalena M Grabowska1, Mark L Day
1Program in Cell and Molecular Biology and the Department of Urology, University of Michigan, Ann Arbor.
Frontiers in Bioscience (Landmark Edition)
|December 29, 2011
Summary
Soluble E-cadherin (sE-cad), a fragment of E-cadherin, is found in various conditions beyond cancer. Its generation by proteases may drive disease progression by disrupting cell adhesion and promoting invasion.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Epithelial (E)-cadherin maintains cell adhesion and polarity.
- Proteolytic cleavage releases soluble E-cadherin (sE-cad), an 80kDa fragment.
- sE-cad is detected in various diseases, including infections and organ failure.
Purpose of the Study:
- To review the generation and implications of soluble E-cadherin.
- To identify proteases and stimuli involved in sE-cad release.
- To explore the physiological consequences of sE-cad accumulation.
Main Methods:
- Literature review of studies on E-cadherin cleavage and sE-cad.
- Identification of proteases (e.g., ADAMs, MMPs, KLK7, plasmin) implicated in sE-cad generation.
- Analysis of in vitro stimuli (e.g., serum withdrawal, cytokines, growth factors) inducing sE-cad release.
Main Results:
- Multiple proteases, including ADAMs, MMPs, KLK7, and plasmin, cleave E-cadherin.
- Diverse stimuli trigger sE-cad generation in vitro.
- sE-cad accumulation is linked to disrupted cell adhesion, increased migration, invasion, and cell signaling.
Conclusions:
- Soluble E-cadherin is a biomarker and potential mediator in various diseases.
- The generation of sE-cad by specific proteases under various stimuli has significant physiological consequences.
- sE-cad may play a role in disease progression through disruption of cellular integrity and promotion of invasive phenotypes.
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