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Notably, anticardiolipin (antiCL) autoantibodies trigger the formation of NETs via Fc receptor IIa (FcRIIa)dependent mechanisms, consequently facilitating a thromboticinflammatory cascade in antiphospholipid syndrome (APS) [171]

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Interestingly however, a more modest effect was seen on GLP-1R endocytosis when -arrestins were ablated, suggesting that the role of desensitization by -arrestins supersedes their role in GLP-1R trafficking

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