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Sigma-Aldrich

Human Plasminogen activator inhibitor-1

liquid, ≥98% (SDS-PAGE), suitable for activity assay

Sinónimos:

PAI 1, SERPINE1, PAI1

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About This Item

UNSPSC Code:
12352202
eCl@ss:
32160405
NACRES:
NA.77

product name

Human Plasminogen activator inhibitor-1, recombinant,

biological source

human

Quality Level

assay

≥98% (SDS-PAGE)

form

liquid

manufacturer/tradename

Chemicon®

technique(s)

activity assay: suitable

impurities

<1 EU/μg endotoxin

NCBI accession no.

UniProt accession no.

shipped in

dry ice

General description

Plasminogen activator inhibitor-1 (PAI-1) is a member of the serine protease inhibitor (serpin) superfamily and a central regulatory protein in the blood coagulation system. PAI-1 is unique among serpins in exhibiting distinct active and inactive (latent) conformations in vivo. Human PAI-1 is a single-chain glycoprotein with a molecular weight of 43 kDa. This inhibitor acts as "bait" for tissue-type and urokinase-type plasminogen activators (tPA and uPA) and protein C. Its rapid interaction with tPA may function as a major control point in the regulation of fibrinolysis. The highly mobile reactive-center loop (RCL) is thought to account for both the rapid inhibiton of plasminogen activators, and the rapid and spontaneous transition of the unstable, active form of PAI-1 into the stable, inactive conformation (t1/2 at 37oC, 2 hours). The inactive form can be partially reactivated by denaturants such as urea, guanidine hydrochloride or SDS. High concentrations of PAI-1 have been associated with human thromboembolic disease. PAI-1 activity may limit the extent of tumor metastasis, since uPA activity is a major contributory factor promoting dissolution of tumor matrix and basement membrane.
The sequence corresponding to amino acids 24 to 402 of human PAI-1 (mature form) tagged with 6xHis on the carboxy-terminal was expressed in E. Coli.

Application

To fully activate the latent PAI-1, the PAI-1 must be incubated in Activation Buffer (2X Activation Buffer: 8 M Guanidine HCl, 40 mM Sodium Acetate, pH 5.6, 400 mM NaCl, 0.2% Tween 20) for 15 to 30 minutes (Sancho, 1994).The recombinant PAI-1 is able to bind to uPA resulting in a SDS-stable complex.

Physical form

Liquid. In 150 mM Na2HPO4, pH 6.6, 500 mM NaCl, 2 mM Glutathione, and 0.01% Tween-80.

Storage and Stability

Store at -80ºC. Thaw on ice and freeze aliquots at -80ºC for longer storage. This product is stable for at least 2 years as supplied. Avoid repeated freeze/thaw cycles.

Analysis Note

Specific Activity: By uPA activity assay, the recombinant PAI-1 contains a mixture of the active and latent forms, with >45% of active form

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Storage Class

10 - Combustible liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

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P M Sherman et al.
The Journal of biological chemistry, 267(11), 7588-7595 (1992-04-15)
Plasminogen activator inhibitor-1 (PAI-1) is a specific inhibitor of the serine proteases tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). To systematically investigate the roles of the reactive center P1 and P1' residues in PAI-1 function, saturation mutagenesis was
Immunocytoprotection after reperfusion with Kv1.3 inhibitors has an extended treatment window for ischemic stroke.
Lee, et al.
Frontiers in Pharmacology, 14, 1190476-1190476 (2023)
Ruth D Lee et al.
Translational stroke research (2023-04-24)
Senicapoc, a small molecule inhibitor of the calcium-activated potassium channel KCa3.1, was safe and well-tolerated in clinical trials for sickle cell anemia. We previously reported proof-of-concept data suggesting that both pharmacological inhibition and genetic deletion of KCa3.1 reduces infarction and
Victor Garcia et al.
Proceedings of the National Academy of Sciences of the United States of America, 117(17), 9497-9507 (2020-04-18)
Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is a critical mediator of vascular function. eNOS is tightly regulated at various levels, including transcription, co- and posttranslational modifications, and by various protein-protein interactions. Using stable isotope labeling with

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