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Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

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DLG1/SAP97 modulates transforming growth factor alpha bioavailability.

Anne-Laure Surena¹, Giselle P de Faria, Jeanne-Marie Studler

¹Inserm, UMR894, University of Paris 5, 75014 Paris, France.

Biochimica Et Biophysica Acta

|October 22, 2008

Summary

This summary is machine-generated.

Discs Large Gene 1 (DLG1) protein interacts with pro-Transforming Growth Factor alpha (pro-TGFalpha) and TACE, influencing TGFalpha shedding. DLG1 plays a dual role in controlling TGFalpha bioavailability in glioma cells.

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Area of Science:

Oncology
Molecular Biology
Cell Signaling

Background:

Transforming Growth Factor alpha (TGFalpha) and its receptor EGFR are implicated in glioma development.
Soluble TGFalpha is generated by TACE/ADAM17-mediated cleavage of its precursor, pro-TGFalpha.
Understanding TGFalpha bioavailability is crucial for targeting gliomas.

Purpose of the Study:

To identify proteins interacting with the intracellular domain of pro-TGFalpha.
To elucidate the role of these interactions in TGFalpha shedding and bioavailability.

Main Methods:

Yeast two-hybrid screening to identify pro-TGFalpha interacting proteins.
In vivo complex detection in U251 glioma cells and glioma-derived tumor-initiating cells.
Manipulation of DLG1 levels to assess its functional impact.

Main Results:

Discs Large Gene 1 (DLG1/SAP97) interacts with intracellular domains of both pro-TGFalpha and TACE via distinct PDZ domains.
A pro-TGFalpha-DLG1-TACE complex exists in glioma cells.
DLG1 exhibits dual functions in pro-TGFalpha shedding, promoting proximity but limiting TACE activity.

Conclusions:

DLG1 is a key regulator of TGFalpha bioavailability.
DLG1 dynamically interacts with pro-TGFalpha and TACE to control TGFalpha shedding.
These findings offer insights into glioma pathogenesis and potential therapeutic targets.