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Related Concept Videos

Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
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Structure of Cadherins01:25

Structure of Cadherins

The cadherins were one of the first cell adhesion molecules discovered; the term “cadherins”   is based on their calcium-dependent adhering properties. The first cadherins discovered on the epithelial, neuronal, and placental cells were named E-cadherin, P-cadherin, and N-cadherin, respectively. These classical cadherins share sequence and structural similarities. Other cadherins, including those involved in cell signaling, are grouped into non-classical cadherins. This diversity of cadherins...
Catenins01:23

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Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
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Actin Polymerization and Cell Motility01:13

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Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
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Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

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E-cadherin mutations and cell motility: a genotype-phenotype correlation.

Ana Rita Mateus1, Joana Simões-Correia, Joana Figueiredo

  • 1Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), 4200-465 Porto, Portugal. amateus@ipatimup.pt

Experimental Cell Research
|March 10, 2009
PubMed
Summary

Germline mutations in the E-cadherin gene (CDH1) impact cell motility and signaling pathways. Specific CDH1 mutations affecting the extracellular domain increase cell motility and may benefit from EGFR inhibitors in Hereditary Diffuse Gastric Cancer.

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Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules
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Published on: October 17, 2014

Related Experiment Videos

Last Updated: Jun 25, 2026

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
03:45

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Published on: August 8, 2022

Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules
08:15

Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules

Published on: October 17, 2014

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • E-cadherin is crucial in suppressing tumor invasion and metastasis.
  • Germline mutations in the CDH1 gene cause Hereditary Diffuse Gastric Cancer (HDGC), with missense mutations comprising 23% of these cases.
  • Previous studies show CDH1 missense mutations can have significant functional consequences.

Purpose of the Study:

  • To investigate how mutations in different E-cadherin protein domains affect cell motility.
  • To explore the impact of eleven specific HDGC CDH1 germline missense mutations on cell motility and associated signaling pathways.

Main Methods:

  • Characterized the effect of eleven HDGC CDH1 germline missense mutations on cell motility.
  • Assessed the activation of signaling pathways including EGFR, Src kinase, and MAPKs in cells with CDH1 mutations.
  • Analyzed mutations located on extracellular and juxtamembrane domains.

Main Results:

  • CDH1 mutations in extracellular and juxtamembrane domains increased cell motility and EGFR activation.
  • Extracellular E-cadherin mutants showed increased activation of Src kinase and p38 MAPK.
  • Identified E-cadherin domains critical for cell motility and established a genotype-phenotype correlation.

Conclusions:

  • E-cadherin domains are pivotal for regulating cell motility.
  • Specific CDH1 mutations correlate with distinct cellular phenotypes.
  • A subset of HDGC patients with extracellular E-cadherin mutations may respond to EGFR inhibitors.