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. Author manuscript; available in PMC: 2023 Mar 15.
Published in final edited form as: Matrix Biol. 2022 Aug 22;112:132–154. doi: 10.1016/j.matbio.2022.08.009

Figure 3. Surface plasmon resonance analysis of competition between HMCN1 and LAMγ1 for NID2 binding.

Figure 3.

LAMγ1 short arm (A) or HMCN1 fragment HMCN1-G2E1-5 (B) were immobilized on the chip surface, and the chip was perfused with 200 nM NID2 (A, a; KD = koff / kon = 6 nM), 200 nM NID2 plus 1 μM HMCN1-G2E1-5 (A, b), 200 nM NID2 plus 2 μM HMCN1-G2E1-5 (A, c), 50 nM NID2 (B, a, red), 50 nM NID2 plus 250 nM LAMγ1 mutant deficient in nidogen binding mutant (N836D; (82,83) (B, b, blue), 50 nM NID2 plus 50 nM LAMγ1 short arm (B, c, green), or 50 nM NID2 plus 250 nM LAMγ1 short arm (B,d, magenta), respectively.