Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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.
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...
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...
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
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...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Effect of feeding Yucca schidigera extract and a live yeast on the rumen microbiome and performance of dairy cows fed a diet excess in rumen degradable nitrogen.

Animal : an international journal of animal bioscience·2023
Same author

Influence of rate of inclusion of microalgae on the sensory characteristics and fatty acid composition of cheese and performance of dairy cows.

Journal of dairy science·2019
Same author

Discovery and characterization of an antibody directed against exosite I of thrombin.

Journal of thrombosis and haemostasis : JTH·2015
Same author

The influence of grass silage-to-maize silage ratio and concentrate composition on methane emissions, performance and milk composition of dairy cows.

Animal : an international journal of animal bioscience·2015
Same author

Thrombin inhibition by the serpins.

Journal of thrombosis and haemostasis : JTH·2013
Same author

Type II antithrombin deficiency caused by a large in-frame insertion: structural, functional and pathological relevance.

Journal of thrombosis and haemostasis : JTH·2012
Same journal

The Natural Mutation Arg221aTrp in Human α-Thrombin Abrogates Physiological Na<sup>+</sup> Binding and Preferentially Hinders the Protease Anticoagulant Functions.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

A historical review of the biological, semantic and clinical aspects of aspirin resistance.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

Association between Thrombus Neutrophil Extracellular Traps Content and Ischemic Stroke Recurrence.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

Peptide-Mediated Inhibition of Surface-Initiated Thrombogenesis.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

Growth differentiation factor-15 and bleeding risk in patients with venous thromboembolism.

Journal of thrombosis and haemostasis : JTH·2026
Same journal

Physiological Anticoagulant Deficiencies: Pathogenesis, Diagnosis, and Clinical Implications.

Journal of thrombosis and haemostasis : JTH·2026
See all related articles

Related Experiment Video

Updated: Jun 21, 2026

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
08:01

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well

Published on: February 27, 2026

Slow thrombin is zymogen-like.

J A Huntington1

  • 1Department of Haematology, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK. jah52@cam.ac.uk

Journal of Thrombosis and Haemostasis : JTH
|July 28, 2009
PubMed
Summary
This summary is machine-generated.

Blood coagulation involves zymogen activation, but initiation is allosteric. Slow thrombin, a zymogen-like protease, is allosterically activated, blurring the lines between zymogens and active enzymes.

More Related Videos

Tracking Fibrinolysis of Chandler Loop-Formed Whole Blood Clots Under Shear Flow in An In-Vitro Thrombolysis Model
06:16

Tracking Fibrinolysis of Chandler Loop-Formed Whole Blood Clots Under Shear Flow in An In-Vitro Thrombolysis Model

Published on: April 19, 2024

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization
06:28

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

Published on: June 4, 2020

Related Experiment Videos

Last Updated: Jun 21, 2026

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
08:01

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well

Published on: February 27, 2026

Tracking Fibrinolysis of Chandler Loop-Formed Whole Blood Clots Under Shear Flow in An In-Vitro Thrombolysis Model
06:16

Tracking Fibrinolysis of Chandler Loop-Formed Whole Blood Clots Under Shear Flow in An In-Vitro Thrombolysis Model

Published on: April 19, 2024

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization
06:28

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

Published on: June 4, 2020

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Physiology

Background:

  • Blood coagulation is a cascade of zymogen activation events.
  • Zymogens are inactive precursors activated by cleavage.
  • Factor VIIa and thrombin exhibit unique activation mechanisms.

Purpose of the Study:

  • To review general features of zymogen activation.
  • To explore protease-like zymogens and zymogen-like proteases.
  • To analyze the allosteric activation of slow thrombin.

Main Methods:

  • Literature review of zymogen activation.
  • Analysis of structural features of slow thrombin.
  • Comparison of zymogen and protease characteristics.

Main Results:

  • Zymogen activation is not always a simple cleavage event.
  • Some zymogens possess inherent activity (protease-like zymogens).
  • Some proteases exist in low-activity states (zymogen-like proteases).

Conclusions:

  • Allosteric activation of thrombin represents a transition from a zymogen-like state to an active serine protease.
  • The distinction between zymogens and proteases is often blurred.
  • Understanding these states is crucial for blood coagulation research.