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Related Experiment Videos

Calreticulin affects beta-catenin-associated pathways.

M P Fadel1, M Szewczenko-Pawlikowski, P Leclerc

  • 1Department of Anatomy and Cell Biology, University of Toronto, Toronto, Ontario M5S 1A8, Canada.

The Journal of Biological Chemistry
|May 23, 2001
PubMed
Summary
This summary is machine-generated.

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Calreticulin overexpression increases cell adhesion by affecting beta-catenin dephosphorylation and potentially impacting the Wnt signaling pathway. This suggests a link between endoplasmic reticulum function and cell adhesion regulation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Calreticulin is an endoplasmic reticulum protein involved in calcium storage and protein folding.
  • Calreticulin is known to influence cell adhesion.
  • The Wnt signaling pathway and cadherin-mediated cell adhesion are critical for tissue development and homeostasis.

Purpose of the Study:

  • To investigate the role of calreticulin in modulating cell adhesiveness.
  • To identify proteins affected by calreticulin overexpression, particularly in relation to cell adhesion.
  • To explore the potential link between calreticulin, protein phosphorylation, and the Wnt signaling pathway.

Main Methods:

  • Overexpression of calreticulin in cells.
  • Assessment of cell adhesiveness.

Related Experiment Videos

  • Analysis of N-cadherin, vinculin, beta-catenin, and tyrosine phosphorylation levels.
  • Postulation of signaling pathway involvement.

    • Main Results:

    • Calreticulin overexpression correlated with increased cell adhesiveness.
    • N-cadherin and vinculin expression were increased with calreticulin overexpression.
    • Tyrosine phosphorylation was decreased, with beta-catenin being notably dephosphorylated.

    Conclusions:

    • Calreticulin influences cell adhesiveness through mechanisms involving beta-catenin dephosphorylation.
    • Calreticulin may impact the Wnt signaling pathway via the cadherin/catenin complex.
    • Endoplasmic reticulum-mediated signaling, involving protein-tyrosine kinases/phosphatases, is implicated in calreticulin's effect on cell adhesion.