Zinc-redox crosstalk regulates proteostasis in the endoplasmic reticulum
inhibits the Ero1α-PDI oxidative system, and that ERp44 enhances this inhibitory effect. Consequently, the ER redox environment becomes more reducing, severely impairing the oxidative folding of key membrane receptors such as Notch1 and EGFR. These findings reveal the essential role of zinc homeostasis in redox-dependent proteostasis within the ER.
Authors
- Kenji Inaba (ORCID: https://orcid.org/0000-0001-8229-0467)
- Yuta Amagai (ORCID: https://orcid.org/0000-0002-2999-4622)
- Masaki Matsumoto (ORCID: https://orcid.org/0000-0002-6987-0288)
- Jun Hoseki
- Roberto Sitia (ORCID: https://orcid.org/0000-0001-7086-4152)
- Satoshi Watanabe (ORCID: https://orcid.org/0000-0002-1130-0477)
- Wakana Yamamoto
- Shin Mizukami (ORCID: https://orcid.org/0000-0002-2292-8606)
- Toshiyuki Kowada (ORCID: https://orcid.org/0000-0002-6623-6505)
- Chihiro Arai
Institutions
- Kyushu University (JP)
- Tohoku University (JP)
- Japan Agency for Medical Research and Development (JP)
- IRCCS Ospedale San Raffaele (IT)
- Niigata University (JP)
- Kyoto University of Advanced Science (JP)
Publication Details
- Journal
- Nature Communications
- Published
- 2026-04-21
- DOI
- https://doi.org/10.1038/s41467-026-72250-w
- Primary Topic
- Trace Elements in Health
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Asahi Glass Foundation
- Japan Agency for Medical Research and Development
- Japan Society for the Promotion of Science London