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Mogues T, Etzerodt M, Hall C, et al. Tetranectin Binds to the Kringle 1-4 Form of Angiostatin and Modifies Its Functional Activity. J Biomed Biotechnol. 2004;2004(2):73-78doi: 10.1155/S1110724304307096.
Mogues, T., Etzerodt, M., Hall, C., Engelich, G., Graversen, J. H., & Hartshorn, K. L. (2004). Tetranectin Binds to the Kringle 1-4 Form of Angiostatin and Modifies Its Functional Activity. Journal of biomedicine & biotechnology, 2004(2), 73-78. https://doi.org/10.1155/S1110724304307096
Mogues, Tirsit, et al. "Tetranectin Binds to the Kringle 1-4 Form of Angiostatin and Modifies Its Functional Activity." Journal of biomedicine & biotechnology vol. 2004,2 (2004): 73-78. doi: https://doi.org/10.1155/S1110724304307096
Mogues T, Etzerodt M, Hall C, Engelich G, Graversen JH, Hartshorn KL. Tetranectin Binds to the Kringle 1-4 Form of Angiostatin and Modifies Its Functional Activity. J Biomed Biotechnol. 2004;2004(2):73-78. doi: 10.1155/S1110724304307096. PMID: 15240916; PMCID: PMC548802.
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J Biomed Biotechnol. 2004;2004(2):73-78. doi: 10.1155/S1110724304307096.

Tetranectin Binds to the Kringle 1-4 Form of Angiostatin and Modifies Its Functional Activity.

Journal of biomedicine & biotechnology

Tirsit Mogues, Michael Etzerodt, Crystal Hall, Georg Engelich, Jonas H. Graversen, Kevan L. Hartshorn

PMID: 15240916 PMCID: PMC548802 DOI: 10.1155/S1110724304307096

Abstract

Tetranectin is a plasminogen kringle 4 domain-binding protein present in plasma and various tissue locations. Decreased plasma tetranectin or increased tetranectin in stroma of cancers correlates with cancer progression and adverse prognosis. A possible mechanism through which tetranectin could influence cancer progression is by altering activities of plasminogen or the plasminogen fragment, angiostatin. Tetranectin was found to bind to the kringle 1-4 form of angiostatin (AST $;{\text{K1-4}}$ ). In addition, tetranectin inhibited binding of plasminogen or AST $;{\text{K1-4}}$ to extracellular matrix (ECM) deposited by endothelial cells. Finally, tetranectin partially counteracted the ability of AST $;{\text{K1-4}}$ to inhibit proliferation of endothelial cells. This latter effect of tetranectin was specific for AST $;{\text{K1-4}}$ since it did not counteract the antiproliferative activities of the kringle 1-3 form of angiostatin (AST $;{\text{K1-3}}$ ) or endostatin. These findings suggest that tetranectin may modulate angiogenesis through interactions with AST.

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