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Since NOX associates with the angiotensin AT-I receptor in lipid rafts [66], it is probable that AT-I receptor agonism activates NOX, generating superoxide signal transduction, perhaps via a mechanism analogous to GPCR signalling or via membrane depolarisation as previously documented in the vasculature [174,175]
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Type 1 immunoglobulin E (IgE)-mediated reactions may occur as the IgE antibody binds to the N1 heterocyclic ring
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