36
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Activation of latent TGF-beta by thrombospondin-1: mechanisms and physiology.

      Cytokine & Growth Factor Reviews
      Animals, Binding Sites, Breast Neoplasms, drug therapy, metabolism, Carcinoma, Extracellular Matrix, ultrastructure, Glomerulonephritis, Membranoproliferative, Humans, Peptide Fragments, Protein Precursors, Proteins, Pulmonary Fibrosis, Rats, Tamoxifen, pharmacology, Thrombospondin 1, physiology, Transforming Growth Factor beta, Transforming Growth Factor beta1, Wound Healing

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Regulation of the activation of latent TGF-beta is essential for health as too much or too little TGF-beta activity can have serious, deleterious consequences. The processes that control conversion of the precursor to the biologically active form of TGF-beta in vivo are not well characterized. We have identified a mechanism for the activation of latent TGF-beta that involves binding of the secreted and extracellular matrix protein, thrombospondin-1 (TSP-1), to the latent precursor. Specific sequences in TSP-1 and in the precursor portion (the latency associate peptide-LAP) have been determined to be essential for activation of latent TGF-beta by TSP-1. It is thought that binding of TSP-1 to the latent complex induces a conformational rearrangement of the LAP in such a manner as to prevent the LAP from conferring latency on the mature domain of TGF-beta. A TSP-dependent mechanism of activation may be locally important during wound healing and in post-natal development of epithelial structures. The possible involvement of TSP-1 in TGF-beta activation during several disease processes is also discussed.

          Related collections

          Author and article information

          Comments

          Comment on this article