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Correlation of SEED sequential parsing median CR with locations of known clinical amino-acid substitutions that cause von Willebrand disease (4). Gain-of-function (type-2B VWD) clinical mutations are R1341Q, P1337L, V1324D, and V1316M. Loss-of-function (type-2M VWD) clinical mutations are E1359K, F1369I, I1425F, A1437T, and R1374H. Allosteric gain-of-function R1450E in α6 helix. To see this figure in color, go online.
