{"refrec":{"BRefID":257693,"RR":"<b>Cuypers, E.; Peigneur, S.; Debaveye, S.; Shiomi, K.; Tytgat, J.</b> (2011). TRPV1 channel as new target for marine toxins: Example of gigantoxin I, a sea anemone toxin acting via modulation of the PLA<sub>2</sub> pathway. <i>Acta Chim. Slov. 58(4)</i>: 735-741","BEntID":249703,"PublicFlag":1,"CheckedFlag":1,"wosflag":1,"vabbflag":null,"RefStringPartII":". <i>Acta Chim. Slov. 58(4)</i>: 735-741","DocTypID":8,"DocType":"Journal article","MarineFlag":1,"FreshFlag":0,"BrackishFlag":0,"TerrestrialFlag":0,"Authorstring":"Cuypers, E.; Peigneur, S.; Debaveye, S.; Shiomi, K.; Tytgat, J.","OrigTitleTranslFlag":0,"Authorstringtrunc":"Cuypers, E. <i>et al.</i>","Englishabstract":"Gigantoxin I, isolated from sea anemone Stichodactyla gigantea, was previously described as the first epidermal growth factor (EGF)-like toxin from natural origin. In this study, we discovered the interaction between the transient receptor potential vanilloid subtype I (TRPV1) channels and gigantoxin I. The TRPV1 channel is a non-selective cation channel involved in pain sensation and is described as pharmacological target of cnidaria venom. Our results highlight the involvement of the epidermal growth factor receptor/phospholipaseA(2)/arachidonic acid/lipoxygenase (EGFR/PLA(2)/AA/LOX) pathway in the indirect activation of TRPV1 channels by gigantoxin I. This is the first time that this pathway is described in the indirect activation of TRPV1 channels by toxins. 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