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The disulfide bridge between the N-terminus and the ECL3 at the end of transmembrane helix (TM) 7, critical for CCL1 signaling activity and conserved in chemokine receptors 34 , is observed in the CCL1-CCR8-Gi structure but absent in our Fab1-CCR8 structure, likely due to disulfide bond instability during protein purification in the absence of chemokine 22,28 (Supplementary Fig

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The amyloid is predominantly composed of protein in a beta-pleated sheet conformation