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Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

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...
Clot Retraction and Fibrinolysis01:16

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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.
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

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 forms a...
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

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...
Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
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Coagulation01:09

Coagulation

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...

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Updated: Jun 8, 2026

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes
12:24

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes

Published on: June 3, 2014

Factor XIII: novel structural and functional aspects.

I Komáromi1, Z Bagoly, L Muszbek

  • 1Clinical Research Center Thrombosis, Haemostasis and Vascular Biology Research Group of the Hungarian Academy of Sciences, University of Debrecen, Medical and Health Science Center, Debrecen, Hungary.

Journal of Thrombosis and Haemostasis : JTH
|October 1, 2010
PubMed
Summary
This summary is machine-generated.

Factor XIII (FXIII) is a crucial enzyme for hemostasis and cellular functions. Its structure and activation mechanisms, particularly the role of FXIII-A and FXIII-B subunits, are key to understanding its diverse biological roles.

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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Enzymology

Background:

  • Factor XIII (FXIII) is a protransglutaminase essential for hemostasis and possesses diverse intracellular functions.
  • Plasmatic FXIII (pFXIII) is a tetramer (FXIII-A2B2), while cellular FXIII (cFXIII) is a dimer (FXIII-A2).
  • FXIII-A shares conserved structural domains with other transglutaminases, while FXIII-B is a glycoprotein composed of sushi domains.

Purpose of the Study:

  • To elucidate the structural elements of FXIII-A involved in FXIII-B interaction.
  • To review the activation process of pFXIII and cFXIII.
  • To present a molecular model of FXIIIa structure and discuss its implications for enzyme activity.

Main Methods:

  • Literature review and analysis of structural and biochemical studies.
  • Molecular modeling based on analogies with transglutaminase-2.
  • Biochemical studies to validate structural models.

Main Results:

  • The first sushi domain of FXIII-B appears critical for complex formation with FXIII-A.
  • pFXIII activation involves thrombin cleavage, Ca(2+) -dependent dissociation of FXIII-B, and fibrinogen acceleration.
  • cFXIII activation bypasses proteolysis.
  • A molecular model of FXIIIa structure was developed, aligning with biochemical findings.

Conclusions:

  • Understanding FXIII structure-function relationships is vital for its roles in hemostasis and cellular processes.
  • The molecular model provides insights into FXIIIa's active conformation and substrate interactions.
  • Further research into FXIII's structural dynamics can illuminate its therapeutic potential.