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 Experiment Videos

Structural and functional correlation of ADAMTS13.

Jing-fei Dong1

  • 1Thrombosis Research Section, Baylor College of Medicine, Houston, TX 77030, USA. jfdong@bcm.tmc.edu

Current Opinion in Hematology
|April 7, 2007
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Extracellular Mitochondria Mediate Endothelial Injury After Traumatic Brain Injury.

Arteriosclerosis, thrombosis, and vascular biology·2026
Same author

Hyperadhesive von Willebrand Factor Contributes to Pathogenesis of Preeclampsia.

Arteriosclerosis, thrombosis, and vascular biology·2026
Same author

A Component Analysis of Endotheliopathy of Trauma.

Research square·2026
Same author

OmicGlaze: Spatial Multi-Omic Mapping of Traumatic Brain Injury.

bioRxiv : the preprint server for biology·2026
Same author

Assessment Of Novel Platform Of Thrombin Generation To Predict Venous Thromboembolism Early After Traumatic Injury: A Prospective Cohort Study.

Shock (Augusta, Ga.)·2026
Same author

Circulating Nucleosomes Are Elevated In Trauma Patients With Venous Thromboembolism: A Prospective Case-Cohort Study.

Shock (Augusta, Ga.)·2026
Same journal

Dynamic myeloid suppressor states in cancer and inflammation and their therapeutic potential.

Current opinion in hematology·2026
Same journal

Factor XIa inhibition for the prevention of thrombosis: mechanism, clinical trial signals, and indication-specific positioning.

Current opinion in hematology·2026
Same journal

Nutrition as a regulator of hematopoietic stem cell biology and transplantation.

Current opinion in hematology·2026
Same journal

From biomimicry to clinical actionability: rethinking high-shear thrombosis as a mechanobiological system.

Current opinion in hematology·2026
Same journal

Bidirectional relationship between metabolic and thrombotic disease mechanisms.

Current opinion in hematology·2026
Same journal

The dual role of the brain-derived neurotrophic factor as a regulator of hemostasis and thrombotic risk.

Current opinion in hematology·2026
See all related articles

Recent research highlights ADAMTS13’s role in preventing thrombotic thrombocytopenic purpura. Understanding ADAMTS13’s interaction with von Willebrand factor is key to treating this condition.

Area of Science:

  • Hematology
  • Molecular Biology
  • Biochemistry

Background:

  • Thrombotic thrombocytopenic purpura (TTP) is a life-threatening condition caused by dysregulated von Willebrand factor (VWF).
  • ADAMTS13, a metalloprotease, plays a critical role in cleaving VWF, thereby preventing thrombosis.

Purpose of the Study:

  • To summarize recent advancements in the understanding of ADAMTS13.
  • To elucidate the mechanisms underlying VWF cleavage and its regulation by ADAMTS13.
  • To explore the potential of ADAMTS13 as a therapeutic agent for TTP and other thrombotic disorders.

Main Methods:

  • Review of recent scientific literature on ADAMTS13.
  • Analysis of structure-function relationships of ADAMTS13 and VWF.
  • Investigation of genetic mutations associated with TTP and von Willebrand disease.

Related Experiment Videos

  • Studies involving ADAMTS13-knockout mouse models.
  • Main Results:

    • The core ADAMTS13-binding site is in the A2 domain, with other domains influencing interaction.
    • Factors like urea, BaCl2, and low ionic strength are crucial for VWF cleavage under static conditions.
    • ADAMTS13 deficiency alone may not be sufficient to cause TTP, suggesting other contributing factors.
    • ADAMTS13 shows potential as an antithrombotic agent for TTP and related conditions.

    Conclusions:

    • ADAMTS13 research has significantly advanced since its characterization.
    • Current knowledge clarifies ADAMTS13's interaction with VWF and TTP pathogenesis.
    • Further understanding of ADAMTS13 is crucial for developing novel therapeutic strategies for thrombotic disorders.