FUT11-Driven fucosylation coordinates K63 ubiquitination of keratin 17 to sustain psoriatic keratinocytes hyperproliferation
Our results indicate that FUT11-driven fucosylation is integral to the stabilization of K17 via K63 ubiquitination, thereby perpetuating psoriatic inflammation. Targeting FUT11 or inhibiting fucosylation with 2-FF presents a novel therapeutic strategy for psoriasis management. This study highlights the critical interplay between glycosylation and ubiquitination in the pathophysiology of psoriasis, positioning FUT11 and K17 as pivotal targets for intervention.
Authors
- Erle Dang (ORCID: https://orcid.org/0000-0003-4761-6673)
- Shuai Shao (ORCID: https://orcid.org/0000-0003-0699-1864)
- Gang Wang (ORCID: https://orcid.org/0000-0002-5842-8080)
- Xia Li (ORCID: https://orcid.org/0000-0001-5478-8970)
- Qingyang Li (ORCID: https://orcid.org/0000-0003-1560-7270)
- Guohao Li
- Haijun Miao (ORCID: https://orcid.org/0009-0009-0477-0567)
- Jixin Gao (ORCID: https://orcid.org/0000-0003-2659-0048)
- Lixin Yue
Institutions
- Xijing Hospital (CN)
- Air Force Medical University (CN)
Publication Details
- Journal
- Cell Communication and Signaling
- Published
- 2025-10-22
- DOI
- https://doi.org/10.1186/s12964-025-02422-6
- Citations
- 1
- Primary Topic
- Skin and Cellular Biology Research
- Type
- article
- Field-Weighted Citation Impact
- 1.15