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Updated: May 17, 2026
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Bead Aggregation Assays for the Characterization of Putative Cell Adhesion Molecules
Published on: October 17, 2014
ALCAM/CD166 adhesive function is regulated by the tetraspanin CD9.
Alvaro Gilsanz1, Lorena Sánchez-Martín, María Dolores Gutiérrez-López
1Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Nicolás Cabrera 1, Campus de Cantoblanco, 28049, Madrid, Spain.
Cellular and Molecular Life Sciences : CMLS
|October 12, 2012
Summary
Activated Cell Adhesion Molecule (ALCAM) interactions are enhanced by the tetraspanin CD9. This CD9-mediated upregulation of ALCAM function boosts cell adhesion, T cell migration, and proliferation.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Activated Cell Adhesion Molecule (ALCAM/CD166) is an immunoglobulin superfamily member mediating cell adhesion via homophilic (ALCAM-ALCAM) or heterophilic (ALCAM-CD6) interactions.
- ALCAM plays critical roles in leukocyte extravasation, immune synapse stabilization, T cell activation, and tumor metastasis.
- The precise mechanisms regulating ALCAM's adhesive capacity remain largely unknown.
Purpose of the Study:
- To elucidate the regulatory mechanisms governing ALCAM's adhesive function.
- To investigate the role of tetraspanin CD9 in modulating ALCAM-mediated interactions.
Main Methods:
- Confocal microscopy for colocalization studies.
- Biochemical analyses to identify protein complexes.
- Functional assays to assess cell adhesion, migration, activation, and proliferation.
Main Results:
- ALCAM directly associates with CD9 and the metalloproteinase ADAM17/TACE on leukocyte surfaces.
- CD9 significantly upregulates both homophilic and heterophilic ALCAM interactions.
- CD9 enhances ALCAM-mediated cell adhesion and T cell responses.
Conclusions:
- CD9 enhances ALCAM function through increased ALCAM clustering and surface expression.
- Inhibition of ADAM17 activity by CD9 contributes to ALCAM surface expression upregulation.
- These findings reveal a novel regulatory pathway for ALCAM function with implications for immune responses and cancer.
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