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The Capital Region of Denmark - a part of Copenhagen University Hospital
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Neutralisation of uPA with a monoclonal antibody reduces plasmin formation and delays skin wound healing in tPA-deficient mice

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  1. GPIHBP1 and Lipoprotein Lipase, Partners in Plasma Triglyceride Metabolism

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  2. Evolution and Medical Significance of LU Domain-Containing Proteins

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  3. The PCNA interaction motifs revisited: thinking outside the PIP-box

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  4. Did evolution create a flexible ligand-binding cavity in the urokinase receptor through deletion of a plesiotypic disulfide bond?

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Proteolytic degradation by plasmin and metalloproteinases is essential for epidermal regeneration in skin wound healing. Plasminogen deficient mice have severely delayed wound closure as have mice simultaneously lacking the two plasminogen activators, urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA). In contrast, individual genetic deficiencies in either uPA or tPA lead to wound healing kinetics with no or only slightly delayed closure of skin wounds.
Original languageEnglish
JournalP L o S One
Volume5
Issue number9
Pages (from-to)e12746
ISSN1932-6203
DOIs
Publication statusPublished - 1 Jan 2010

ID: 32222753