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Related Concept Videos

Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
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...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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.
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
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...
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: May 9, 2026

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
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Structural basis for the stabilization of the complement alternative pathway C3 convertase by properdin.

Martín Alcorlo1, Agustín Tortajada, Santiago Rodríguez de Córdoba

  • 1Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, 28040 Madrid, Spain.

Proceedings of the National Academy of Sciences of the United States of America
|August 1, 2013
PubMed
Summary

Properdin stabilizes complement C3/C5 convertases on pathogens by cross-linking components. This structural stabilization enhances innate immunity and prevents host tissue damage during infection.

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Area of Science:

  • Immunology
  • Structural Biology
  • Biochemistry

Background:

  • Complement system is crucial for innate immunity.
  • Unstable C3/C5 convertases mediate inflammation and lysis.
  • Regulatory proteins prevent host damage by inactivating convertases.

Purpose of the Study:

  • To elucidate the mechanism by which properdin stabilizes C3/C5 convertases.
  • To understand properdin's role in innate immunity on pathogen surfaces.

Main Methods:

  • Electron microscopy was used to visualize properdin-convertase complexes.
  • Structural analysis of properdin oligomers and their interactions with C3b and Bb.

Main Results:

  • Properdin oligomers form a 'curly vertex' that binds C3b and Bb, stabilizing the convertase.
  • Properdin induces conformational changes in C3b, hindering inactivation by regulatory proteins.
  • This stabilization enhances complement amplification on pathogen surfaces.

Conclusions:

  • Properdin acts as a molecular scaffold, stabilizing C3/C5 convertases through cross-linking and structural reorganization.
  • This mechanism ensures efficient complement-mediated pathogen clearance while protecting host tissues.