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Related Concept Videos

Structure of Cadherins01:25

Structure of Cadherins

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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...
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Cadherins in Tissue Organization01:19

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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.
Cell Sorting During Development
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Catenins01:23

Catenins

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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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Desmosomes01:05

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The term desmosome derives from the Greek words "desmo" and "soma" meaning "adhesion bodies." This structure was first observed during the late 1800s and described as small, dense nodules in the epidermis. Desmosomes are button-like structures that help form an interlinked network of intermediate filaments across the cells. These junctions are  essential to hold cells together under mechanical stress and to maintain tissue integrity. Desmosomes are multi-protein...
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Adherens Junctions01:24

Adherens Junctions

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Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
Adherens Junctions are Dynamic
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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Related Experiment Video

Updated: Aug 30, 2025

Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules
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Roads to Stat3 Paved with Cadherins.

Hanad Adan1, Juliet Daniel1, Leda Raptis2

  • 1Department of Biology, McMaster University, Hamilton, ON L8S 4L8, Canada.

Cells
|August 26, 2022
PubMed
Summary

Cadherin engagement activates Rac/Cdc42 GTPases, promoting IL6 cytokine secretion and Stat3 activation. This pathway, involving cadherins, Rac, and gp130, is crucial for cell division and survival, with implications for cancer drug development.

Keywords:
FAKIL6SrcStat3cadherinscaveolin-1cell densitygp130rac1

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Related Experiment Videos

Last Updated: Aug 30, 2025

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Cadherins mediate cell-cell adhesion and influence intracellular signaling pathways.
  • Signal transducer and activator of transcription-3 (Stat3) is a key regulator of cell division and survival.
  • The interplay between cadherins, GTPases, and Stat3 in cellular processes is not fully understood.

Purpose of the Study:

  • To elucidate the role of cadherin engagement in the activation of Stat3 signaling.
  • To investigate the molecular mechanisms linking cadherins, Rac/Cdc42 GTPases, and IL6 family cytokines to Stat3.
  • To explore the potential therapeutic implications of the cadherin-Stat3 axis in cancer.

Main Methods:

  • Investigated the effect of cadherin engagement on Rac/Cdc42 GTPase activity and proteasomal degradation.
  • Assessed the impact of cadherin signaling on IL6 family cytokine secretion and gp130 receptor activation.
  • Analyzed Stat3 phosphorylation, dimerization, nuclear translocation, and target gene activation.
  • Examined the role of Src oncogene and caveolin-1 in modulating the cadherin-Stat3 pathway.

Main Results:

  • Cadherin engagement increases Rac/Cdc42 GTPase activity by inhibiting proteasomal degradation, leading to IL6 cytokine secretion and autocrine gp130 activation.
  • This cascade results in Stat3 phosphorylation, dimerization, nuclear translocation, and activation of genes involved in cell division and survival.
  • Src oncogene and caveolin-1 modulate this pathway, highlighting a critical balance between Src, cadherins, and gp130 for Stat3 activation.
  • Absence of cadherin engagement leads to low Stat3 activity, emphasizing the importance of cadherin-gp130 interaction for Stat3 signaling.

Conclusions:

  • Cadherin engagement is essential for Stat3 activation, primarily through the preservation of gp130 function and regulation of the Rac/gp130 axis.
  • A delicate balance between Src, cadherins, and IL6 signaling is required for optimal Stat3 activation.
  • The cadherin-Rac-gp130 pathway represents a conserved mechanism for Stat3 activation with significant implications for cancer biology and drug development.