The TGF-β co-receptor, CD109, promotes internalization and degradation of TGF-β receptors

62Citations
Citations of this article
64Readers
Mendeley users who have this article in their library.

Abstract

Transforming growth factor-β (TGF-β) is implicated in numerous pathological disorders, including cancer and mediates a broad range of biological responses by signaling through the type I and II TGF-β receptors. Internalization of these receptors via the clathrin-coated pits pathway facilitates SMAD-mediated signaling, whereas internalization via the caveolae pathway is associated with receptor degradation. Thus, molecules that modulate receptor endocytosis are likely to play a critical role in regulating TGF-β action. We previously identified CD109, a GPI-anchored protein, as a TGF-β co-receptor and a negative regulator of TGF-β signaling. Here, we demonstrate that CD109 associates with caveolin-1, a major component of the caveolae. Moreover, CD109 increases binding of TGF-β to its receptors and enhances their internalization via the caveolae. In addition, CD109 promotes localization of the TGF-β receptors into the caveolar compartment in the presence of ligand and facilitates TGF-β-receptor degradation. Thus, CD109 regulates TGF-β receptor endocytosis and degradation to inhibit TGF-β signaling. This article is part of a Special Issue entitled: 11th European Symposium on Calcium. © 2011 Elsevier B.V.

Cite

CITATION STYLE

APA

Bizet, A. A., Liu, K., Tran-Khanh, N., Saksena, A., Vorstenbosch, J., Finnson, K. W., … Philip, A. (2011). The TGF-β co-receptor, CD109, promotes internalization and degradation of TGF-β receptors. Biochimica et Biophysica Acta - Molecular Cell Research, 1813(5), 742–753. https://doi.org/10.1016/j.bbamcr.2011.01.028

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free