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Christopher M. Overall

Researcher at University of British Columbia

Publications -  314
Citations -  31412

Christopher M. Overall is an academic researcher from University of British Columbia. The author has contributed to research in topics: Matrix metalloproteinase & Proteases. The author has an hindex of 90, co-authored 302 publications receiving 28860 citations. Previous affiliations of Christopher M. Overall include University of Toronto & Canadian Institutes of Health Research.

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Strategies for MMP inhibition in cancer: innovations for the post-trial era

TL;DR: It is now recognized that MMP activity is tightly regulated at several levels, providing new avenues for blocking these enzymes and leading to new therapeutic strategies for cancer.
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Validating matrix metalloproteinases as drug targets and anti-targets for cancer therapy

TL;DR: The matrix metalloproteinases mediate homeostasis of the extracellular environment and have multiple signalling activities that are commonly altered during tumorigenesis and that might serve as intervention points for anticancer drugs.
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Multi-step pericellular proteolysis controls the transition from individual to collective cancer cell invasion

TL;DR: Both ECM track widening and transition to multicellular invasion are dependent on MT1-MMP-mediated collagenolysis, shown by broad-spectrum protease inhibition and RNA interference, and invasive migration and proteolytic ECM remodelling are interdependent processes that control tissue micropatterning and macrop atterning.
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Human and mouse proteases: a comparative genomic approach

TL;DR: The availability of the human and mouse genome sequences has allowed the identification and comparison of their respective degradomes — the complete repertoire of proteases that are produced by these organisms.
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Inflammation dampened by gelatinase A cleavage of monocyte chemoattractant protein-3.

TL;DR: Cleaved MCP-3 binds to CC-chemokine receptors-1, -2, and -3, but no longer induces calcium fluxes or promotes chemotaxis, and instead acts as a general chemokine antagonist that dampens inflammation, suggesting that matrix metalloproteinases are both effectors and regulators of the inflammatory response.