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Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: Biophysical mapping of TREM2-ligand interactions reveals shared surfaces for engagement of multiple Alzheimer’s disease ligands

Fig. 5

C1q binding to TREM2 is mainly disrupted by TREM2 basic site variants. Immobilized TREM2 was probed for binding to C1q (62.5–1000 nM). (A) Scheme of experiment. (B-N) BLI sensorgrams for C1q binding to TREM2 (B) WT, (C) M41D, (D) L69D, (E) W70D, (F) L71D, (G) F74D, (H) L89D, (I) L69D/L71D, (J) W44D/L69D/L71D, (K) R46A/R47A, (L) R46A, (M) R46D, (N) R76D, (O) R77D, (P) R47H, (Q) R62H, (R) T96K, (S) L75D, (T) T85D, (U) R122D/K123D. Black = BLI sensorgrams; red = 1:1 kinetic fits. Results shown in Table 2. (V-X) Summary of BLI steady-state binding response versus concentration for C1q binding to TREM2 (V) hydrophobic site variants and (X) basic site variants

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Molecular Neurodegeneration

ISSN: 1750-1326