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Fig. 8. A schematic outlining the relationships between metalloproteinases, metalloproteinase inhibitors and regulators of 
-catenin signaling. In Timp3+/+ setting, E-cadherin and GSK3 influence the cytoplasmic pool of -catenin, which can translocate into the nucleus and function as transcriptional co-activator for target genes, Ccnd1 (cyclin D1) and Mmp7. We propose that MMP and ADAM activity operates upstream of E-cadherin and GSK3 through yet unidentified mechanisms to influence the signaling pool of -catenin. In Timp3 deficient mammary epithelial cells, -catenin signaling activity is increased, leading to selective gene responses. These arise in a GSK3-dependent manner and are not influenced by E-cadherin blocking. (
, increased expression or activity; 
, decreased expression or activity; 
, unchanged expression or activity.)
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