Molecular dynamics simulations corroborate recombinant expression studies carried out on three αIIb β-propeller mutations reported in Indian Glanzmann thrombasthenia patients.

Abstract excerpt

Mutations in the αIIb β-propeller domain have long been known to disrupt heterodimerization and intracellular trafficking of αIIbβ3 complexes leading to diminished surface expression and/or function, resulting in Glanzmann thrombasthenia. Our previous study on three β-propeller mutations, namely G128S, S287L, and G357S, showed variable defects in protein transport correlated with the patient's clinical...

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