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Updated: May 8, 2026

Production of Pseudotyped Particles to Study Highly Pathogenic Coronaviruses in a Biosafety Level 2 Setting
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Naturally occurring ACE2 stalk variants are differentially released from the cell.

Florian Wiersch1, Christine Lux1, Julia Vanderliek-Kox1

  • 1Institute of Molecular Pharmacology, Medical Faculty, RWTH Aachen University, Aachen, Germany.

Biorxiv : the Preprint Server for Biology
|May 7, 2026
PubMed
Summary
This summary is machine-generated.

The ACE2 stalk region significantly influences ectodomain shedding, affecting soluble ACE2 release. Specific mutations, like P734L, increase ACE2 surface expression and B0AT1 levels, impacting physiological roles.

Keywords:
ADAM10ADAM17SNPsrenin-angiotensin-aldosterone systemsoluble ACE2

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Physiology

Background:

  • Angiotensin-converting enzyme 2 (ACE2) regulates the renin-angiotensin-aldosterone system (RAAS) and serves as the SARS-CoV-2 receptor.
  • ACE2 stabilizes the B0AT1 amino acid transporter, making its surface expression critical for physiological functions.
  • Ectodomain shedding, mediated by ADAM10 and ADAM17, releases soluble ACE2, but regulatory mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the role of the ACE2 stalk region in ectodomain shedding.
  • To identify specific mutations affecting ACE2 release and surface expression.
  • To understand how B0AT1 complex formation influences ACE2 shedding.

Main Methods:

  • Analysis of 11 naturally occurring single-point mutations in the ACE2 stalk region.
  • Quantification of soluble ACE2 release compared to wild-type (WT) ACE2.
  • Assessment of surface ACE2 and B0AT1 levels.

Main Results:

  • Most ACE2 stalk variants showed reduced release; P734L and G726R mutations significantly increased release.
  • The ACE2_P734L mutation led to higher surface expression of both ACE2 and B0AT1.
  • Complex formation between ACE2 and B0AT1 did not impede ACE2 shedding by sheddases.

Conclusions:

  • The ACE2 stalk region is a key determinant of ectodomain shedding efficiency.
  • Naturally occurring ACE2 variants can alter soluble ACE2 release, potentially contributing to interindividual pathophysiological differences.
  • Shedding regulation is independent of ACE2-B0AT1 complex stability.