Improving tissue-type plasminogen activator (tPA) thrombolytic therapy is a high priority in stroke research. The ability of tPA to convert plasminogen efficiently into clot-dissolving plasmin relies on an endogenous fibrinolytic assembly via a triple complex formation of tPA, annexin A2, and plasminogen. Annexin A2 is a cell-surface protein, which, in complex with its binding partner p11, form...