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These results suggest that the extracellular matrix genes are new therapeutic targets for invasive tumors.
We have shown that Sox9 activity and expression of cartilage matrix genes are limited by coincident activation of NF-κB and RARs.
Unfortunately many of these key matrix genes are expressed in a variety of mesenchymal tissues and therefore may not be sufficiently discriminatory.
Representative images are shown in Figure 2. Chondrocyte differentiation and the expression of cartilage matrix genes are in part regulated by Sox transcription factors [ 42].
Cluster analysis and heat map of the expression of phase I genes, phase II genes, inflammatory genes, genes involved in cell signaling and apoptosis, ubiquitin-proteasome complex genes, growth factors, and extracellular matrix genes are shown in Figure 3.
To construct a reference network from the matrix, genes are treated as nodes, and an edge is drawn between two genes if they share at least one common attribute.
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A limitation of our study is that a role for the miR-29 and miR-15 family MREs in the CDS of elastin and other matrix genes was not demonstrated in an in vivo model system.
Cartilage-specific matrix genes were found to be modulated by rhOP-1 treatment.
However, the general histological structure and expression of matrix genes was not affected (Fig. 6c).
Microaarray analysis provided evidence that 27 extracellular matrix genes were differentially regulated in diabetes.
In contrast, the other three specific eggshell matrix genes were expressed only in the uterus as expected.
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