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Related Concept Videos

Coagulation01:06

Coagulation

1.5K
Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
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Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

2.6K
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
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Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

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Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
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Coagulation01:09

Coagulation

8.4K
The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
8.4K
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

10.9K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
10.9K
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

6.0K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
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Related Experiment Video

Updated: May 1, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

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Concanavalin A inhibits tissue factor coagulant activity.

F A Pitlick

    The Journal of Clinical Investigation
    |January 1, 1975
    PubMed
    Summary

    Concanavalin A (con A) reversibly inhibits tissue factor coagulant activity by binding to a carbohydrate residue. This inhibition is reversed by alpha-methyl-D-glucoside, suggesting the apoprotein provides the carbohydrate.

    Area of Science:

    • Biochemistry
    • Hematology
    • Molecular Biology

    Background:

    • Tissue factor initiates the extrinsic pathway of blood coagulation.
    • Concanavalin A (con A) is a lectin known to bind carbohydrates.
    • The interaction of con A with tissue factor's coagulant activity is not fully understood.

    Purpose of the Study:

    • To investigate the mechanism by which Concanavalin A (con A) inhibits tissue factor coagulant activity.
    • To determine if the inhibition is reversible and dependent on carbohydrate binding.
    • To identify the role of the tissue factor apoprotein in this interaction.

    Main Methods:

    • Assessing the effect of con A on native tissue factor coagulant activity.
    • Testing the reversibility of con A inhibition using alpha-methyl-D-glucoside.

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    Related Experiment Videos

    Last Updated: May 1, 2026

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    Author Spotlight: High-Sensitivity Tissue Factor Activity Assay for Plasma Diagnosis
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  • Incubating con A with tissue factor in the presence of alpha-methyl-D-glucose.
  • Recombining purified tissue factor apoprotein with various phospholipids and assessing con A inhibition.

    • Main Results:

    • Concanavalin A (con A) potently and reversibly inhibits the coagulant activity of native tissue factor.
    • Inhibition by con A is reversed upon addition of alpha-methyl-D-glucoside.
    • Coagulant activity is preserved if alpha-methyl-D-glucose is present during con A incubation.
    • Purified tissue factor apoprotein, when recombined with phospholipids, is also reversibly inhibited by con A.

    Conclusions:

    • Concanavalin A (con A) inhibits tissue factor coagulant activity through reversible binding to a carbohydrate residue.
    • The tissue factor apoprotein likely provides the carbohydrate moiety involved in the con A interaction.
    • These findings elucidate a novel regulatory mechanism for tissue factor activity.