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Medical device thrombosis involves Factor XII (FXII) activation. Targeting FXII surface binding sites, revealed by structural modeling, may prevent device-related clotting without altering essential protein functions.

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Area of Science:

  • Biochemistry
  • Structural Biology
  • Biophysics

Background:

  • Medical device-associated thrombosis is a significant clinical issue.
  • Thrombosis can be initiated by Factor XII (FXII) binding to artificial surfaces and subsequent contact pathway activation.
  • Understanding FXII structure is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the structural properties of full-length Factor XII (FXII) using the AlphaFold model.
  • To identify potential targets for selective pharmacological blockade of FXII in medical device-associated thrombosis.
  • To explore how FXII conformation influences its activation and surface binding.

Main Methods:

  • Utilized the AlphaFold Protein Structure Database for a model of full-length FXII.
  • Integrated the AlphaFold model with existing structure-function data.
  • Analyzed intramolecular interactions and their effect on the FXII cleavage site (R353).

Main Results:

  • The AlphaFold model reveals FXII adopts a three-point harness-like conformation.
  • Intramolecular interactions bury the R353 cleavage site, maintaining zymogen quiescence.
  • Positively charged surface patches, likely involved in anionic surface binding, are exposed.
  • Surface binding and antibodies induce conformational changes that accelerate FXII activation.

Conclusions:

  • The structural model provides insights into FXII auto-inhibition and activation mechanisms.
  • Targeting surface binding sites is a promising strategy for preventing medical device-associated thrombosis.
  • Therapeutic strategies should aim to block surface interactions without inducing detrimental structural changes.