Since its emergence in late 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been spreading remarkably fast worldwide. Effective countermeasures require the rapid development of data and tools to monitor its spread and better understand immunogenic profile. However, limited information is available about the tools and target of the immune responses to SARS-CoV-2.
View Article and Find Full Text PDFRationale: Current thrombolytic agents activate plasminogen to plasmin which triggers fibrinolysis to dissolve thrombi. Since plasmin is a nonspecific proteolytic enzyme, all of the current plasmin-dependent thrombolytics lead to serious hemorrhagic complications, demanding a new class of fibrinolytic enzymes independent from plasmin activation and undesirable side effects. We speculated that the mammalian version of bacterial heat-shock proteins could selectively degrade intravascular thrombi, a typical example of a highly aggregated protein mixture.
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