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Related Concept Videos

Gap Junctions01:27

Gap Junctions

The cytoplasm of adjacent animal cells can exchange small molecules, ions, and secondary messengers via the communication channels which form the gap junctions. These junctions comprise a few hundred to thousands of molecular channels, each made of two halves, called the connexon hemichannel. A connexon is a hexamer of six transmembrane connexin proteins, which assemble radially, thus forming a pore or channel in the center. One connexon hemichannel docks with a corresponding connexon on the...
Gap Junctions01:37

Gap Junctions

Multicellular organisms employ a variety of ways for cells to communicate with each other. Gap junctions are specialized proteins that form pores between neighboring cells in animals, connecting the cytoplasm between the two, and allowing for the exchange of molecules and ions. They are found in a wide range of invertebrate and vertebrate species, mediate numerous functions including cell differentiation and development, and are associated with numerous human diseases, including cardiac and...
Overview of Cell-Matrix Interactions01:24

Overview of Cell-Matrix Interactions

The extracellular matrix or ECM holds cells together to form a tissue and allows the cells within the tissue to communicate. ECM comprises proteins such as fibronectin, collagen, laminin, etc. The most abundant protein in this space is collagen. Collagen fibers are interwoven with carbohydrate-containing protein molecules called proteoglycans. ECM allows cell migration and provides a structural scaffold at cell adhesion that anchors the cell when the extracellular matrix proteins interact with...

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Related Experiment Video

Updated: Jun 21, 2026

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption
09:20

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption

Published on: October 4, 2019

Exogenous Cx43 expression decrease cell proliferation rate in rat hepatocarcinoma cells independently of functional

Marisa Ionta1, Raphael Adolpho Sant'ana Ferreira, Sandra Cristina Pfister

  • 1Department of Cell and Developmental Biology, Institute of Biomedical Science University of Sao Paulo, Brazil. ionta@usp.br

Cancer Cell International
|August 15, 2009
PubMed
Summary
This summary is machine-generated.

Exogenous Connexin 43 (Cx43) expression reduced hepatocellular carcinoma cell proliferation and reversed transformed phenotypes, independent of gap junction intercellular communication (GJIC). These findings suggest Cx43

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A Functional Assay for Gap Junctional Examination; Electroporation of Adherent Cells on Indium-Tin Oxide
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Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption
09:20

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Gap Junctional Intercellular Communication: A Functional Biomarker to Assess Adverse Effects of Toxicants and Toxins, and Health Benefits of Natural Products
05:27

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A Functional Assay for Gap Junctional Examination; Electroporation of Adherent Cells on Indium-Tin Oxide
11:02

A Functional Assay for Gap Junctional Examination; Electroporation of Adherent Cells on Indium-Tin Oxide

Published on: October 18, 2014

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Gap junction intercellular communication (GJIC) is crucial for homeostasis, regulating cell proliferation and differentiation.
  • Reduced GJIC is observed in solid tumors, and its restoration can revert the transformed phenotype.
  • Recent studies suggest connexin expression alone may revert malignancy.

Purpose of the Study:

  • To investigate the effects of exogenous Connexin 43 (Cx43) expression on rat hepatocarcinoma cell proliferation and phenotype.

Main Methods:

  • Transfection of rat hepatocarcinoma cells with exogenous Cx43.
  • Assessment of GJIC capacity.
  • Evaluation of cell proliferation rate, actin filament organization, cell morphology, and substrate adhesion.

Main Results:

  • Exogenous Cx43 expression did not enhance GJIC capacity.
  • Cx43 significantly decreased cell proliferation rate.
  • Cx43 induced actin filament reorganization, cell flattening, and increased substrate adhesion.

Conclusions:

  • Cx43 expression reduces hepatocellular carcinoma cell growth and reverts the transformed phenotype.
  • These effects are independent of GJIC capacity.
  • Cx43-mediated reversion may involve changes in phosphorylation patterns and protein redistribution.