Literature summary for 3.4.21.73 extracted from

Nassar, T.; Yarovoi, S.; Fanne, R.; Waked, O.; Allen, T.; Idell, S.; Cines, D.; Higazi, A.
Urokinase plasminogen activator regulates pulmonary arterial contractility and vascular permeability in mice (2011), Am. J. Respir. Cell Mol. Biol., 45, 1015-1021.

Search for more literature for 3.4.21.73

Protein Variants

Protein Variants	Comment	Organism
additional information	generation of an uPA PAI-I docking-site mutant	Homo sapiens

Inhibitors

Inhibitors	Comment	Organism	Structure
PAI-1	-	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining

Synonyms

Synonyms	Comment	Organism
uPA	-	Homo sapiens
Urokinase plasminogen activator	-	Homo sapiens

General Information

General Information	Comment	Organism
malfunction	at pathophysiological concentrations above 20 nM, uPA inhibits contractility and increases vascular permeability	Homo sapiens
additional information	urokinase plasminogen activator is elevated in pathological settings such as acute lung injury, where pulmonary arterial contractility and permeability are disrupted	Homo sapiens
physiological function	uPA limits the accretion of fibrin after lung injury. uPA regulates the in vitro pulmonary arterial contractility induced by phenylephrine in a dose-dependent manner through two receptor-dependent pathways, and regulates vascular contractility and permeability in vivo. Physiological concentrations of uPA below 1 nM stimulate the contractility of pulmonary arterial rings induced by phenylephrine through the low-density lipoprotein receptor-related protein receptor. The pro-contractile effect of uPA is independent of its catalytic activity. The inhibition of vascular contractility and increase of vascular permeability is mediated through a two-step process that involves docking to N-methyl-Daspartate receptor-1 on pulmonary vascular smooth muscle cells, and requires catalytic activity	Homo sapiens

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Release 2023.1 (January 2023)