An isoform of 14‐3‐3 protein regulates transbilayer lipid movement at the plasma membrane
-NBD-PS). However, 14-3-3 zeta knockdown does not further enhance PS resistance in ATP11C-deficient cells. These findings indicate that 14-3-3 zeta plays a regulatory role in ATP11C-dependent transbilayer movement of PS at the plasma membrane. Impact statement 14-3-3ζ regulates ATP11C-dependent phosphatidylserine (PS) transbilayer movement at the plasma membrane. Reduced 14-3-3ζ impairs PS flipping and confers resistance to exogenous PS in CHO cells, identifying 14-3-3ζ as a key modulator of phospholipid asymmetry and lipid-induced cytotoxicity.
Authors
- Toshihide Kobayashi (ORCID: https://orcid.org/0000-0002-4811-7270)
- Akiko Yamaji‐Hasegawa (ORCID: https://orcid.org/0000-0002-8058-2076)
- Akira Hattori (ORCID: https://orcid.org/0000-0001-5509-2326)
- Masafumi Tsujimoto
Institutions
- Centre National de la Recherche Scientifique (FR)
- Teikyo Heisei University (JP)
- Kyoto Pharmaceutical University (JP)
- RIKEN Center for Brain Science (JP)
- RIKEN (JP)
- RIKEN Center for Biosystems Dynamics Research (JP)
- Japan Bio Products (Japan) (JP)
- RIKEN Advanced Science Institute (JP)
- Université de Strasbourg (FR)
- Kyoto University of Advanced Science (JP)
Publication Details
- Journal
- FEBS Letters
- Published
- 2026-04-15
- DOI
- https://doi.org/10.1002/1873-3468.70338
- Primary Topic
- 14-3-3 protein interactions
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Ministry of Education, Culture, Sports, Science and Technology
- RIKEN