Takanori Aoki

TL;DR: It is demonstrated that MT1‐MMP forms a homophilic complex through the hemopexin‐like (PEX) domain that acts as a mechanism to keep MT1-MMP molecules close together to facilitate proMMP‐2 activation.

TL;DR: It is demonstrated for the first time that CTGF is a substrate of MMPs and that the angiogenic activity of VEGF165 suppressed by the complex formation withCTGF is recovered through the selective degradation of CTGF by M MPs.

TL;DR: It is demonstrated for the first time that MT-MMP-1 is a gelatinolytic enzyme and secreted from cells in a complex with TIMP-2, which can form a ternary complex ofMT-M MP-1/TIMP2/proMMP -2.

TL;DR: It is demonstrated that vascular maturation coordinated by endothelial cell/mural cell interactions redirects MT1-MMP expression to the neovessel tip where the protease regulates matrix remodeling at the leading edge of the developing vasculature.

TL;DR: TIMP‐3 is a potent inhibitor against the aggrecanase activity of ADAMTS4 in vivo, suggesting that the inhibitory activity of tissue inhibitors of metalloproteinases to ADAMts4 is a key role in the degradation of aggreca in arthritides.