TFPI Antibodies

Tissue factor pathway inhibitor (TFPI)

Inhibits factor X (X(a)) directly and, in a Xa-dependent manner, inhibits VIIa/tissue factor activity, presumably by forming a quaternary Xa/LACI/VIIa/TF complex. It owns an antithrombotic action and also the capability to connect with lipoproteins in plasma.

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Gene Information

Human
Gene Name:	TFPI
Uniprot:	P10646
Entrez:	7035

Family

Belongs to:
No superfamily

Alternative Names

convertin; EPI; EPITFPI1LACITFI; Extrinsic pathway inhibitor; LACI; Lipoprotein-associated coagulation inhibitor; TFPI; tissue factor pathway inhibitor (lipoprotein-associated coagulation inhibitor); tissue factor pathway inhibitor

Molecular Weight

Mass (kDA):
35.015 kDA

Genomic Context

Human
Location:	2q32.1
Sequence:	2; NC_000002.12 (187464230..187554505, complement)

Tissue Specificity

Mostly in endothelial cells.

Subcellular Localizations

[Isoform Alpha]: Secreted.; [Isoform Beta]: Microsome membrane; Lipid-anchor, GPI-anchor.

Diseases

• Thrombosis
• Blood Coagulation Disorders
• Thrombophilia
• Inflammation
• Hemorrhage
• Venous Thrombosis
• Neoplasms
• Malignant Neoplasms
• Systemic Infection
• Thrombus
• Von Willebrand Disease
• Disseminated Intravascular Coagulation
• Infarction

• Atherosclerosis
• Cardiovascular Diseases
• Thromboembolism
• Myocardial Infarction
• Tumor Angiogenesis
• Deep Vein Thrombosis
• Neoplasm Metastasis

Pathways

• Coagulation
• Blood Coagulation
• Fibrinolysis
• Hemostasis
• Pathogenesis
• Angiogenesis
• Localization
• Secretion
• Cell Proliferation
• Platelet Activation
• Proteolysis
• Inflammatory Response
• Platelet Aggregation

• Cell Adhesion
• Regulation Of Coagulation
• Glycosylation
• Excretion
• Cell Migration
• Tube Formation
• Endocytosis

PTMs

• Cleavage
• Phosphorylation
• Glycosylation
• Oxidation
• Gpi Anchoring
• Reduction

• Acetylation
• Sulphation
• Methylation
• Iodination
• Nitration
• Biotinylation

• Deglycosylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TFPI

Best Uses Of The TFPI Marker

The TFPI marker can be used to determine the presence of a protein that has a modulatory effect on hemophilia bleeding. This marker can be used to determine the presence of hemophilia. The protein can be used by researchers around the globe for a variety of reasons, including to submit results for species, applications or for special samples. This is a global program that is accessible to researchers of all nationalities and experience levels.

A TFPI modulator of bleeding in hemophilia

In a mouse model of hemophilia in mice, the absence of TFPI decreased bleeding from the tail, suggesting the possibility of TFPI as a hemostasis modulator. By inhibiting TFPI could also aid in improving hemostasis in FVIII mice with a deficiency. However, the mechanism behind this isn't yet fully identified. However, hemophilia A/B research have revealed that inhibition of TFPI activity can reduce the severity of bleeding.

TFPI is found within the hematopoietic cell and has been demonstrated to reduce bleeding after trauma to the vascular system, in mice with hemophilia. The results of a different study have revealed that TFPI is a physiological regulator of bleeding. It has a significant role in controlling bleeding in hemophilia patients. Further research is needed to confirm that TFPI is responsible for this effect.

TFPI is produced by a variety of alternatively spliced isoforms, with each one having its own distinct function. Adult tissues produce TFPIb in all major vascular beds, while mouse platelets produce TFPIa in a highly evolved conserved form. It is possible that platelet-specific production will result in more efficient production of thrombin. The pharmacological agents that block TFPI in hemophilia are under development for the treatment of hemophilia.

Significant implications for bleeding disorders have been revealed by the discovery of TFPIa as a modulator of hemophilia. The inhibitor inhibits the tissue factor-activated factor 7 complex (TFa) through its first Kunitz domain and FXa through its second Kunitz domain. The study also found that TFPIa may be biologically relevant. A low level of TFPIa in humans could increase the risk of vein thrombosis as well as coronary heart disease.

In mice with hemophilia B a decrease in TFPI activity reduces the loss of tail blood after vascular injury. In addition an additional antibody might be required to stop sequestered pools of TFPI. In addition, a decrease of the loss of blood from the tail in Tfpi+/ mice resulted in a greater fibrin deposition. The effect was observed in a larger number of platelet clots as opposed to mice lacking the hematopoietic cell TFPI protein.

There are a number of limitations with intravenous factor replacement. Because of the shorter half-life of recombinant factor, frequent injections are necessary. Patients who have limited venous access might face inhibitor development, making frequent injections difficult. The quality of life of patients is also affected by frequent injections. These issues could be addressed by the latest hemophilia treatments.

The results suggest that the absence of functional TFPI causes an apparent consumptive coagulopathy during development. Mice lacking functional TFPI do not survive embryogenesis. FVIII deficiency can, however be unable to save embryos or Tfpi. A mouse model of hemophilia indicates that an unrestrained activation (FX) can trigger an irreparable blood coagulopathy which can be fatal to embryonic development.

Its significance in the treatment of hemophilia as a modulator of bleeding

TFPI which is tissue factor pathway inhibitor, could be described as an anticoagulant protein that blocks the activity of prothrombinase. By inhibiting TFPI can restore functional hemostasis by an extrinsic bloodcoagulation pathway. This is independent of factors VIII and IX. Therefore having a comprehensive understanding of the structure and biochemistry of TFPI is crucial for the development of therapeutic agents that are effective.

Anti-TFPI therapies could represent an advancement in the treatment of haemophilia. Anti-TFPIs have bioavailability and stable pharmacokinetics. They can also effectively prevent bleeds in haemophilia A and B patients, which includes those on inhibitors. They may also be applicable to patients who do not have inhibitors.

Hemophilia is caused due to a variety of proteins. The FVIII gene is on the X chromosome. It has six large introns. This gene could cause severe hemophilia when it is transversed intraonically. The FIX gene is more resistant to mutations and is less. While the TFPI gene is smaller and less susceptible to mutation It is also important to keep in mind that the TFPI gene is closely linked to the FVIII gene. A study of the royal family in Bulgaria discovered that Alexi had hemophilia. His treatment had a significant influence on the revolution of 1917.

These results suggest that TFPIa reduces the activity of prothrombinase. A further investigation of this pathway in patients will lead to new understanding of bleeding and thrombotic disorders. It could also prove useful in the development of targeted new treatments. The TFPI marker's significance as a modulator of bleeding in hemophilia

Recombinant factor VIIa is a successful intravenous therapy for hemophilia A. It is also well tolerated and reduces the requirement for rescue therapy. The medication does not trigger an immune response in patients with hemophilia. Its low thrombogenicity may help it gain momentum in the hemophilia treatment field.

The TFPI marker blocks blood coagulation at the beginning stages. It interacts with factor VIIa and activates platelets to form fibrin networks. These proteins are later converted to thrombin and eventually form clots. TFPI blocks the early forms prothrombinase in blood coagulation.

Its use as a marker for hemophilia

Hemophilia A mutations are usually associated with a high likelihood of bleeding, particularly following surgery. A recent study has found that the incidence of bleeding following dental extractions is significantly higher than that of patients who do not suffer from the disease. The frequency of clotting abnormalities is closely related to the clotting activity of FVIII and FIX genes. Hemophilia is a condition that can manifest as mild to severe cases in men Hemophilia carriers often don't show any symptoms.

Hemophilia can easily be diagnosed and treated through genetic testing. A prenatal diagnosis and accurate identification of the carrier can aid in preventing the child from developing the disease. Hemophilia organizations offer genetic counseling and assistance for patients. They also provide numerous support services to improve your health. This article was written by an independent author who has no financial affiliation with any business or person. There is no conflict of interest in the subject matter.

Four chromosome X loci have been identified as STR markers. One of these loci is located near the coagulation factor VIII gene (F8). The STR HA472-CTT-repeat(CATT) is located next to the GAB3 gene. STR HA544 -CTT-repeat x (ATT), y is located 375 kb from the 5'-end of the F8 gene.

Hemophilia is a type of bleeding disorders that are caused by genetic mutations in coagulation factor. Symptoms of this condition include bleeding that occurs spontaneously in internal organs, soft tissues, and joints. The disorder affects about of 20,000 people in United States, and treatment is both preventative and acute. The severity and severity of hemophilia will determine the treatment.

Hemophilia A, a frequent genetic disorder, is caused by a defect in factor VIII. X-linked recessive hemophilia can be clearly inheritable. Its severity is determined by the blood levels of the clotting factor VIII. Patients with mild hemophilia are more likely to bleed excessively following minor trauma. Patients with severe hemophilia will bleed frequently even after minor injuries, such as a minor cut. The severe hemophilia can cause a lot of bleeding of the muscles and joints.

Although hemophilia A is caused by mutations in the factor VIII gene it only affects one male out of the ten thousand males. It is a very costly disease and is of a small size that makes the it crucial to identify carriers. In developing countries indirect linking analysis (ILA) is a viable method to detect carriers. A recent study from the Kurdistan region of Iraq recruited 227 individuals from 41 families. This study proved that hemophilia diagnoses can be confirmed using genetic markers of the factor VIII gene.