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Recent advances in factor XII structure and function.

Aleksandr Shamanaev1, Maxim Litvak, David Gailani

  • 1Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.

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|August 2, 2022
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Summary
This summary is machine-generated.

Factor XII (FXII) normally exists in a closed state, resistant to activation. Surface binding via the EGF1 domain disrupts this, enhancing FXII activation and contributing to thrombosis and angioedema.

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Hematology

Background:

  • Factor XII (FXII) is a key initiator of the contact activation pathway.
  • FXII activation contributes to pathological processes such as angioedema and thrombosis.
  • Understanding FXII structure-function relationships is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the structure-function relationships of Factor XII (FXII).
  • To elucidate the mechanisms regulating FXII activation and its role in disease.
  • To explore the potential of modulating FXII activity for therapeutic benefit.

Main Methods:

  • Utilized recombinant FXII variants with domain replacements from pro-hepatocyte growth factor activator (Pro-HGFA).
  • Assessed FXII activation and activity in solution and on negatively charged surfaces.
  • Investigated the role of specific FXII domains (fibronectin type-2, kringle, EGF1) in activation kinetics and surface binding.

Main Results:

  • Pro-HGFA domain replacements accelerated FXII and prekallikrein activation in solution.
  • FXII and prekallikrein reciprocal activation is enhanced on negatively charged surfaces.
  • The FXII EGF1 domain is essential for surface binding, which promotes activation.

Conclusions:

  • Proposed a model where FXII is normally in an inactive, closed conformation.
  • Surface binding via EGF1 disrupts intramolecular interactions, opening FXII for activation.
  • These findings offer insights into FXII's role in thrombo-inflammatory disorders and potential therapeutic strategies.