HRP Anti-Tissue Plasminogen Activator antibody [EPR7232(2)]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

Tissue Plasminogen Activator (tPA) also known as a plasminogen activator acts mechanically to convert plasminogen to plasmin a serine protease. This reaction occurs at the surface of a fibrin clot leading to clot degradation a process known as fibrinolysis. tPA has a molecular mass of approximately 70 kDa. It is mainly expressed in vascular endothelial cells and is released into the bloodstream in response to stimuli such as circulatory stasis or endothelial damage.

Biological function summary

TPA plays a critical role in thrombolysis by breaking down blood clots into their soluble components. It regulates plasminogen function by cleaving this zymogen to yield the active protease plasmin. This function makes tPA integral in maintaining hemostasis and it does not form a part of a larger protein complex. The activity and the regulation of tPA are important for preventing pathologic clotting which can lead to cardiovascular complications.

Pathways

TPA is central to the fibrinolytic pathway. This pathway facilitates the conversion of plasminogen to plasmin enabling clot resolution. In addition tPA interacts with other proteins such as urokinase plasminogen activator (uPA) and inhibitors like plasminogen activator inhibitor-1 (PAI-1). The balance between tPA and its inhibitors is important for the regulation of fibrinolytic activity impacting hemostatic and thrombotic events.

Associated diseases and disorders

TPA connects closely with conditions like stroke and myocardial infarction due to its thrombolytic properties. In ischemic stroke excessive or insufficient tPA activity can disrupt normal blood flow leading to tissue damage. Additionally in myocardial infarction tPA's role in breaking down clots proves important for restoring coronary blood flow. It is also linked with proteins like fibrinogen as they serve as substrates in the clot degradation process and with PAI-1 which modulates its activity and influences disease progression.