Making sense of latent TGFβ activation

By Justin P. Annes, J. Munger, D. Rifkin. Journal of Cell Science, 2003

1,549 citations recorded by the source corpus.

Subfields: Immunology and Allergy, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/344d712bb128211ae2fd2c60df29754d1b989fae

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Citations in the corpus

The myofibroblast matrix: implications for tissue repair and fibrosis (2013, background): “In mammals, these functions are mediated by the widely expressed three isoforms TGF- 1, TGF- 2 and TGF- 3 that are encoded by three different genes of high homology [119].”
Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix (2007, background): “…can be found at: JCB • VOLUME 179 • NUMBER 6 • 2007 1312 binding to other ECM components like fi brillin-1 and fi bronectin (FN; Unsold et al., 2001; Annes et al., 2003; Hyytiainen et al., 2004; Koli et al., 2005), of which ED-A FN is the major splice variant expressed by Mfs (Serini et al.,…”
SPECIFICITY AND VERSATILITY IN TGF-β SIGNALING THROUGH SMADS (2005, background): “The activities of TGF-β family members are often regulated by secreted and matrixassociated proteins that bind the ligands in solution, thus sequestering the ligands from access to their receptors or helping to ensure ready availability (Annes et al. 2003).”
A syndrome of altered cardiovascular, craniofacial, neurocognitive and skeletal development caused by mutations in TGFBR1 or TGFBR2 (2005, background): “The TGFβs are a family of multipotential cytokines that influence diverse cellular fates including proliferation, migration, synthetic repertoire and deat”
Extracellular control of TGFβ signalling in vascular development and disease (2007, background): “Consistent with these potential mechanisms, all three TGFβ isoforms (TGFβ1, TGFβ2 and TGFβ3 in mammals) are secreted in latent forms that need to be activated before they can bind to signalling receptor”
The extracellular matrix modulates the hallmarks of cancer (2014, positive): “In this regard, the metastatic potential of a transformed cell is favored by an epithelial to mesenchymal transition (EMT), which is fostered by exposure to TGF-b secreted by infiltrating immune cells or via localized degradation of the ECM [91–95].”
Transforming Growth Factor (TGF)-β signaling in cardiac remodeling (2010, background): “Activation of a small fraction of latent TGF-β is capable of generating maximal cellular response [2].”
Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease. (2018, background): “MMPs also activate transforming growth factor-h (TGF-h) by cleaving off the latency-associated peptide (Annes et al., 2003).”
The role of TGF-β Signaling in Myocardial Infarction and Cardiac Remodeling (2007, background): “Most tissues contain significant amounts of latent TGF-β; activation of only a small fraction of this latent TGF-β generates maximal cellular response [ 3 ].”
TGF-β Activation and Function in Immunity (2013, background): “The functions of the different isoforms appear to be similar in vitro, but the diversity of phenotypes of knockout mice for each isoform suggests distinct functions for the isoforms in vivo (5).”