Regulation of the Bioavailability of TGF-β and TGF-β-Related Proteins

  1. Daniel B. Rifkin1,2
  1. 1Departments of Cell Biology, New York University School of Medicine, New York, New York 10016
  2. 2Departments of Medicine, New York University School of Medicine, New York, New York 10016
  1. Correspondence: ian.butler.robertson{at}gmail.com; Daniel.Rifkin{at}nyumc.org

Abstract

The bioavailability of members of the transforming growth factor β (TGF-β) family is controlled by a number of mechanisms. Bona fide TGF-β is sequestered into the matrix in a latent state and must be activated before it can bind to its receptors. Here, we review the molecules and mechanisms that regulate the bioavailability of TGF-β and compare these mechanisms with those used to regulate other TGF-β family members. We also assess the physiological significance of various latent TGF-β activators, as well as other extracellular modulators of TGF-β family signaling, by examining the available in vivo data from knockout mouse models and other biological systems.



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