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Documenti fondamentali

SRP6458

Sigma-Aldrich

TFPI human

recombinant, expressed in HEK 293 cells, ≥95% (SDS-PAGE)

Sinonimo/i:

EPI, LACI, TFI, TFPI1

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About This Item

Codice UNSPSC:
12352202
NACRES:
NA.32

Origine biologica

human

Ricombinante

expressed in HEK 293 cells

Tag

6-His tagged (C-terminus)

Saggio

≥95% (SDS-PAGE)

Stato

lyophilized

Potenza

<0.35 nM IC50

PM

calculated mol wt 30 kDa
observed mol wt 41-45 kDa (DTT-reduced. Protein migrates due to glycosylation. Asp 29 is the predicted N-terminal.)

Confezionamento

pkg of 10 μg

Impurezze

<1 EU/μg endotoxin (LAL test)

N° accesso UniProt

Condizioni di spedizione

wet ice

Temperatura di conservazione

−20°C

Informazioni sul gene

human ... TFPI(7035)

Descrizione generale

The TFPI (tissue factor pathway inhibitor) gene is mapped to human chromosome 2q32.1. This protein exists in two isoforms TFPIα and TFPIβ.
Tissue factor pathway inhibitor (TFPI) also known as Extrinsic pathway inhibitor (EPI), Lipoprotein - associated coagulation inhibitor (LACI), is a plasma proteinase inhibitor synthesized by vascular endothelial cells and part of it is associated with glycosaminoglycans of these cells. TFPI is a single-chain polypeptide which can reversibly inhibit Factor Xa (Xa) and Thrombin (Factor IIa). TFPI is a secreted protein with a N­terminal acidic region, three Kunitz (K) domains separated with by two linker regions, and a C­terminal basic region. The first K domain inhibits coagulation factor VIIa complexed to tissue factor (TF); The second K domain inhibits factor Xa; The third K domain binds to heparin; The C­terminal basic region may have several functions. For example, it plays an important role in binding of TFPI to cell surfaces.

Azioni biochim/fisiol

Inhibition of tissue factor function and thrombus formation by TFPI (tissue factor pathway inhibitor) is a major reason for ischemic stroke in carotid artery disease. The main function of TFPI is to regulate blood coagulation system. It possess both anticoagulant and antimetastatic action. This protein is prominently localized to medial and neointimal smooth muscle cells, macrophages and T-cells of atherosclerotic plaques. Upregulation of the TFPI gene is observed in atherosclerosis. Mutation in the TFPI gene leads to the risk of coronary artery disease.

Stato fisico

Lyophilized from 0.22 μm filtered solution in PBS, pH 7.4. Normally Mannitol or Trehalose is added as protectants before lyophilization.

Ricostituzione

Centrifuge the vial prior to opening. Reconstitute in sterile PBS, pH 7.4 to a concentration of 50 μg/mL. Do not vortex. This solution can be stored at 2-8°C for up to 1 month. For extended storage, it is recommended to store at -20°C.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


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Association analysis of tissue factor pathway inhibitor polymorphisms and haplotypes with osteonecrosis of the femoral head in the Korean population.
Dai XH, et al.
Molecular genetics and metabolism reports, 26(5) (2008)
Tissue Factor Pathway Inhibitor Gene Polymorphism- 33T C Predicts Improved Disease-Free Survival in Colorectal Cancer
Bazzarell AK, et al.
Annals of Surgical Oncology, 23(7), 2274-2280 (2016)
Harald Haidl et al.
Scientific reports, 9(1), 8014-8014 (2019-05-31)
Healthy neonates exhibit a well-functioning haemostatic system despite peculiarities regarding composition of clotting factors and inhibitors as well as impaired platelet aggregation. Thrombocytopenia and severe bleeding events are feared in sick infants. Recombinant factor VIIa (rFVIIa) is a haemostatic agent
Increased expression of TFPI in human carotid stenosis
Stavik B, et al.
Thrombosis Research, 155(5), 31-37 (2017)
Shoko Furukawa et al.
International journal of hematology, 109(4), 390-401 (2019-02-14)
Factor VIIa/tissue factor (FVIIa/TF) initiates blood coagulation by promoting FXa generation (extrinsic-Xa). Subsequent generation of intrinsic FXa (intrinsic-Xa) amplifies thrombin formation. Previous studies suggested that FVIIa/TF activates FVIII rapidly in immediate coagulation reactions, and FVIIa/TF/FXa activates FVIII prior to thrombin-dependent

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