What is Pai-1 4G 5G?

A deletion/insertion polymorphism (4G or 5G) in the promoter of the plasminogen activator inhibitor type 1 (PAI-1) gene is suggested to be involved in regulating the synthesis of the inhibitor, 4G allele, being associated with the enhanced gene expression and plasma PAI-1 levels.

How common is Pai-1 4G 5G?

TABLE 2. PAI-1 Genotypes and PAI-1 Allele Frequencies in Stroke Cases and Controls

Study A Study B
Stroke Patients Stroke Patients
PAI-1 allele frequency
4G 0.66 0.61
5G 0.34 0.39

What is PAI1 deficiency?

Plasminogen activator inhibitor type 1 (PAI1) deficiency is a rare bleeding disorder that causes excessive or prolonged bleeding due to blood clots being broken down too early. PAI1 is a protein in the body needed for normal blood clotting.

What is 4G4G?

The 4G4G genotype of the plasminogen activator inhibitor 4G/5G gene polymorphism is associated with coronary atherosclerosis in patients at high risk for this disease. Thromb Haemost.

What is PAI polymorphism?

The PAI-1 4G/5G polymorphism is a DNA sequence variation that plays a key role in regulating PAI-1 gene expression. Studies have shown that the PAI-1 activity of the 4G allele promoter is higher than that of the 5G allele promoter in a cytokine-stimulated state.

What is Hypofibrinolysis?

Hypofibrinolysis causes impaired clot break-down, leading to thrombosis. This can be caused by the production of auto-antibodies against plasminogen activators (such as tPA and uPA), or against fibrinolytic receptor components (such as annexin).

What is 4G 4G polymorphism?

The 4G/5G polymorphism is a common polymorphism in the promoter region of the PAI-1 gene. 10. Both the 4G and 5G alleles have a binding site for an activator of transcription. The 5G allele, however, has an additional binding site for a repressor, resulting in lower transcription rates and less PAI-1 activity.

Is protein C deficiency a blood disorder?

Protein C deficiency is a disorder that increases the risk of developing abnormal blood clots; the condition can be mild or severe. Individuals with mild protein C deficiency are at risk of a type of blood clot known as a deep vein thrombosis (DVT).

How does PAI-1 affect pregnancy?

During a healthy pregnancy, PAI-1 levels in the plasma gradually elevate during the second trimester of pregnancy and reach a maximum at 32–40 weeks of pregnancy. Within 5–8 weeks after delivery, PAI-1 levels fall again to the levels before the occurrence of pregnancy [2].

What is the process of fibrinolysis?

Fibrinolysis is the enzymatic breakdown of fibrin in blood clots. Plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases. Primary fibrinolysis is a normal body process.

How is the 4G polymorphism of the PAI-1 gene related to pregnancy?

The number of pregnancies (P = .0001) and 4G/4G polymorphism of the PAI-1 gene (P = .029) were positively associated with complications of pregnancy by stepwise logistic regression when the age, number of pregnancies, and all 4 gene mutations were the explanatory variables.

Is the PAI-1 gene a risk factor for thrombosis?

Although the common 4G/5G polymorphism in the promoter of the PAI-1 gene was suggested to be a risk factor for some of the thrombotic disorders, its significance in the development of thrombosis is still controversial. This study presents the data on a total of 357 patients with different types of t …

Where is the PAI-1 gene located on the chromosome?

PAI-1 is an essential protein critical in down-regulation of the fibrinolytic pathway. The protein: PAI-1 is a 47kDa protein and is a member of the serine protease inhibitor (SERPIN) superfamily. The PAI-1 gene in humans is located on chromosome 7q21.3-22, spans approximately 12kb, and consists of nine exons.

Is the PAI-1 gene a reversible heritable risk factor for pregnancy?

Heritable hypofibrinolysis, mediated by 4G/4G homozygosity for the PAI-1 gene, is an independent significant, potentially reversible risk factor for pregnancy complications, probably acting through thrombotic induction of placental insufficiency.