Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

IQGAP1 and calmodulin modulate E-cadherin function.

Z Li1, S H Kim, J M Higgins

  • 1Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston Massachusetts 02115, USA.

The Journal of Biological Chemistry
|December 23, 1999
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Correspondence.

Buffalo medical journal·2023
Same author

Correspondence.

Buffalo medical journal·2023
Same author

Flightless anchors IQGAP1 and R-ras to mediate cell extension formation and matrix remodeling.

Molecular biology of the cell·2020
Same author

Disturbance in sugar metabolism in a three months' old infant.

Guthrie Clinic bulletin·2010
Same author

Ulcerative colitis of unexplained origin.

Guthrie Clinic bulletin·2010
Same author

Differential effects of mineral dusts on the in vitro activation of alveolar macrophage eicosanoid and cytokine release.

Toxicology in vitro : an international journal published in association with BIBRA·2010
Same journal

Isotope-Edited ESEEM: A New Method for Probing Copper Binding Sites in Neurodegenerative Proteins.

The Journal of biological chemistry·2026
Same journal

Introduction to the Thematic Review Series on Intracellular Protein Degradation. The ubiquitous biology of intracellular protein degradation: a tribute to Alfred L. ("Fred") Goldberg.

The Journal of biological chemistry·2026
Same journal

Correction: Aromatic residue-rich amino-terminal segments of temporin L self-assemble into collagen-mimetic peptides with cell-adhesion properties.

The Journal of biological chemistry·2026
Same journal

YhbO is a DJ-1 family glyoxalase and α-oxoaldehyde hydratase that confers resistance to reactive carbonyl stress (112).

The Journal of biological chemistry·2026
Same journal

ARMH3 acts as a central scaffold at the Golgi/TGN through interactions with Arl5, GBF1, and PI4KB.

The Journal of biological chemistry·2026
Same journal

PAX8 controls proximal tubule epithelial identity and stress response through epigenetic modification of distal regulatory elements.

The Journal of biological chemistry·2026
See all related articles

Calmodulin and E-cadherin compete for binding to IQGAP1, a protein crucial for cell adhesion. Blocking calmodulin enhances IQGAP1’s interaction with E-cadherin, impairing cell-cell adhesion.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cadherin proteins mediate calcium-dependent cell-cell adhesion through homophilic interactions.
  • IQGAP1 is a cytoskeletal protein that interacts with actin, Rho family proteins, and E-cadherin.
  • Calmodulin binds to IQGAP1, regulating its association with Cdc42 and actin.

Purpose of the Study:

  • To investigate the competitive binding between calmodulin and E-cadherin for IQGAP1.
  • To determine the role of E-cadherin in IQGAP1 localization at cell junctions.
  • To elucidate the effect of calmodulin antagonism on E-cadherin-mediated cell adhesion.

Main Methods:

  • In vitro binding assays to assess protein interactions.
  • Immunocytochemistry in E-cadherin positive (MCF-7) and negative (MDA-MB-231) cells.

Related Experiment Videos

  • Treatment with a cell-permeable calmodulin antagonist (CGS9343B).

    • Main Results:

    • Calmodulin and E-cadherin compete for binding to IQGAP1.
    • E-cadherin is necessary for IQGAP1 accumulation at cell-cell junctions.
    • Calmodulin antagonism increased IQGAP1 at cell junctions and decreased E-cadherin levels.
    • Calmodulin antagonism impaired homophilic E-cadherin adhesion.

    Conclusions:

    • Disrupting calmodulin binding to IQGAP1 enhances IQGAP1 association with the cadherin-catenin complex.
    • This interaction impairs E-cadherin-mediated cell-cell adhesion.
    • IQGAP1 acts as a molecular link between calmodulin signaling and E-cadherin function.