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Related Experiment Video

Updated: May 19, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

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Published on: October 27, 2020

Matrix control of transforming growth factor-β function.

Masahito Horiguchi¹, Mitsuhiko Ota, Daniel B Rifkin

¹Departments of Cell Biology and Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA. masahito.horiguchi@nyumc.org

Journal of Biochemistry

|August 28, 2012

Summary

This summary is machine-generated.

The extracellular matrix (ECM) sequesters latent transforming growth factor-beta (TGF-β). Loss-of-function mutations paradoxically increase TGF-β levels, challenging current understanding of TGF-β regulation.

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Published on: July 21, 2021

Area of Science:

Biochemistry
Cell Biology
Molecular Biology

Background:

Transforming growth factor-beta (TGF-β) is a crucial cytokine with diverse physiological and pathological roles.
TGF-β requires release from a tripartite complex and binding to its receptor for activity.
Latent TGF-β is sequestered in the extracellular matrix (ECM), essential for its mobilization and activation.

Purpose of the Study:

To review recent findings on the interplay between TGF-β, ECM molecules, and latent TGF-β activation.
To propose a model that resolves the 'TGF-β paradox' observed in ECM-related mutations.

Main Methods:

Literature review of studies investigating TGF-β, ECM interactions, and latent TGF-β activation.
Analysis of loss-of-function mutation data in ECM proteins binding TGF-β.
Development of a theoretical model to explain observed TGF-β levels.

Main Results:

Loss-of-function mutations in ECM proteins binding TGF-β lead to unexpectedly elevated TGF-β levels.
This observation contradicts the expected outcome of reduced TGF-β availability.
The ECM plays a complex role in regulating TGF-β bioavailability and activation.

Conclusions:

The 'TGF-β paradox' highlights the intricate regulatory mechanisms of TGF-β within the ECM.
A proposed model aims to reconcile the observed data and provide a new framework for understanding TGF-β-ECM interactions.
Further research is needed to fully elucidate the complex dynamics of latent TGF-β activation and ECM regulation.