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Related Concept Videos

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.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
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...
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.
Fibronectins Connect Cells with ECM01:25

Fibronectins Connect Cells with ECM

Fibronectin is an adhesive glycoprotein present in the extracellular matrix of embryogenic and adult tissue. These molecules primarily aid in regulating cell motility and attachment. A fibronectin molecule is composed of two identical polypeptide chains attached to each other by a pair of disulfide bonds at the C-terminal.
Both proteoglycans and collagen are attached to fibronectin proteins, which, in turn, are attached to integrin proteins. These integrin proteins interact with transmembrane...
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...
Fibril-associated Collagen01:11

Fibril-associated Collagen

Fibril-associated collagens are a type of collagens present in the extracellular matrix with interrupted triple helices or FACIT (Fibril-associated collagens interrupted triple-helices). FACIT help connect and attach the collagen fibrils with each other as well as with other proteins of the extracellular matrix.
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...

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Related Experiment Video

Updated: Jun 5, 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

FUT8-Dependent Core Fucosylation: Essential for Platelet Function and a Target in Thrombosis.

Ruey-Bing Yang1,2,3, Cheng-Fen Tu1,4, Yan-Ting Chen1

  • 1Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan (R.-B.Y., C.-F.T., Y.-T.C., C.-D.T., F.-A.L.).

Arteriosclerosis, Thrombosis, and Vascular Biology
|June 4, 2026
PubMed
Summary

Fucosyltransferase 8 (FUT8) promotes platelet activation and thrombus formation by adding core fucose to platelet receptors. Inhibiting FUT8 reduces platelet aggregation and protects against thrombosis, suggesting FUT8 as a therapeutic target for cardiovascular diseases.

Keywords:
acetylglucosamineadhesion receptorcardiovascular diseasesfucoseplatelet aggregation

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Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
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Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice

Published on: April 2, 2013

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Last Updated: Jun 5, 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

Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
11:18

Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice

Published on: April 2, 2013

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Hematology

Background:

  • Fucosyltransferase 8 (FUT8) mediates core fucosylation of N-glycans on surface receptors, influencing cellular signaling.
  • Core fucosylation impacts ligand binding and downstream signaling in various cellular contexts.
  • The role of FUT8 in platelet activity and its potential as an antithrombotic target remain to be fully elucidated.

Purpose of the Study:

  • To investigate the presence and role of core fucosylation in platelet adhesion receptors.
  • To determine the impact of core fucosylation on platelet receptor affinity, activation, and signaling.
  • To evaluate the therapeutic potential of FUT8 inhibition in thrombosis models.

Main Methods:

  • Utilized genetic, biochemical, glycomics, and glycoproteomics approaches to identify core fucosylated N-glycans on platelet receptors.
  • Employed binding assays, platelet aggregometry, and phospho-specific antibodies to assess the effects of core fucosylation on platelet function.
  • Investigated the in vivo effects of genetic and pharmacological FUT8 inhibition using murine thrombosis models.

Main Results:

  • Identified core fucosylated N-glycans on platelet receptors, including GPVI and integrin αIIbβ3.
  • Demonstrated that core fucosylation enhances GPVI and αIIbβ3 binding affinity and promotes platelet activation and downstream signaling.
  • Showcased that platelet-specific Fut8 deletion and FUT8 inhibition with FDW028 significantly reduced platelet activation, thrombus formation, and protected against lethal thrombosis in mice.

Conclusions:

  • FUT8-mediated core fucosylation of platelet receptors is a key driver of platelet activation and thrombus formation.
  • FUT8 in platelets represents a promising therapeutic target for managing thrombosis-related cardiovascular diseases.
  • Genetic and pharmacological inhibition of FUT8 offers a viable antithrombotic strategy.