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Vasilakaki, Sofia; Barbayianni, Efrosini; Magrioti, Victoria; Pastukhov, Oleksandr; Constantinou-Kokotou, Violetta; Huwiler, Andrea; Kokotos, George (2016). Inhibitors of secreted phospholipase A2 suppress the release of PGE2 in renal mesangial cells. Bioorganic & medicinal chemistry, 24(13), pp. 3029-3034. Elsevier 10.1016/j.bmc.2016.05.017
Pastukhov, Oleksandr; Schalm, Stephanie; Zangemeister-Wittke, Uwe; Fabbro, Doriano; Bornancin, Frederic; Japtok, Lukasz; Kleuser, Burkhrad; Pfeilschifter, Josef; Huwiler, Andrea (2014). The ceramide kinase inhibitor NVP-231 inhibits breast and lung cancer cell proliferation by inducing M phase arrest and subsequent cell death. British journal of pharmacology, 171(24), pp. 5829-5844. Wiley-Blackwell 10.1111/bph.12886
Pastukhov, Oleksandr; Schalm, Stephanie; Römer, Isolde; Pfeilschifter, Josef; Huwiler, Andrea; Zangemeister-Wittke, Uwe (2014). Ceramide kinase contributes to proliferation but not to prostaglandin E2 formation in renal mesangial cells and fibroblasts. Cellular physiology and biochemistry, 34(1), pp. 119-133. Karger 10.1159/000362989
Huwiler, Andrea; Feuerherm, Astrid J; Sakem, Benjamin; Pastukhov, Oleksandr; Filipenko, Iuliia; Nguyen, Thuy; Johansen, Berit (2012). The ω3-polyunsaturated fatty acid derivatives AVX001 and AVX002 directly inhibit cytosolic phospholipase A(2) and suppress PGE(2) formation in mesangial cells. British journal of pharmacology, 167(8), pp. 1691-701. Oxford: Wiley-Blackwell 10.1111/j.1476-5381.2012.02114.x
Huwiler, Andrea; Bourquin, Florence; Kotelevets, Nataliya; Pastukhov, Oleksandr; Capitani, Guido; Grütter, Markus G; Zangemeister-Wittke, Uwe (2011). A prokaryotic S1P lyase degrades extracellular S1P in vitro and in vivo: implication for treating hyperproliferative disorders. PLoS ONE, 6(8), e22436. Lawrence, Kans.: Public Library of Science 10.1371/journal.pone.0022436
Huwiler, Andrea; Kotelevets, Nataliya; Xin, Cuiyan; Pastukhov, Oleksandr; Pfeilschifter, Josef; Zangemeister-Wittke, Uwe (2011). Loss of sphingosine kinase-1 in carcinoma cells increases formation of reactive oxygen species and sensitivity to doxorubicin-induced DNA damage. British journal of pharmacology, 162(2), pp. 532-43. Oxford: Wiley-Blackwell 10.1111/j.1476-5381.2010.01053.x
