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A 12(s)-Hete Receptor in Lewis Lung Carcinoma Cells

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Lipoxygenases and their Metabolites

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 447))

Abstract

Arachidonic acid is metabolized by at least two distinct 12-lipoxygenases to 12(S)-hydroxy-5, 8,10,14-eicosatetraenoic acid (12(S)-HETE). is produced by several kinds of cells and tissues, e.g. platelets, macrophages, smooth muscle cells, tumor cells, keratinocytes, and by brain tissue (2). It is the major arachidonic acid metabolite in platelets but the precise biological function of this compound in platelets is unknown. It has been suggested that 12(S)-HETE influences platelet adhesion and aggregation (3), has a pathophysiological role in psoriasis (4) , and modulates postsynaptic responses to histamine (5) . 12(S)-HETE also increases tumor cell adhesion to endothelium, subendothelial matrix and fibronectin (6). Moreover, it has recently been reported that 12(S)-HETE is an important regulator of cell survival and apoptosis by modulating the expression of bcl-2 protein (7).

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© 1999 Kluwer Academic/Plenum Publishers, New York

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Herbertsson, H., Kühme, T., Hammarström, S. (1999). A 12(s)-Hete Receptor in Lewis Lung Carcinoma Cells. In: Nigam, S., Pace-Asciak, C.R. (eds) Lipoxygenases and their Metabolites. Advances in Experimental Medicine and Biology, vol 447. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4861-4_18

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  • DOI: https://doi.org/10.1007/978-1-4615-4861-4_18

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-0-306-46044-9

  • Online ISBN: 978-1-4615-4861-4

  • eBook Packages: Springer Book Archive

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