A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Mechanosensitive interactions between Jag1 and Myo1c control Jag1 trafficking in endothelial cells
Tekijät: Stassen, Oscar M. J. A.; Virtanen, Noora; Lin, Kai-Lan; Suarez Rodriguez, Freddy; Heijmans, Matthijs J. M.; Zhao, Feihu; Corthals, Garry L.; Bouten, Carlijn V. C.; Sahlgren, Cecilia M.
Kustantaja: Cell Press
Julkaisuvuosi: 2025
Lehti: iScience
Artikkelin numero: 113879
Vuosikerta: 28
Numero: 12
eISSN: 2589-0042
DOI: https://doi.org/10.1016/j.isci.2025.113879
Julkaisun avoimuus kirjaamishetkellä: Avoimesti saatavilla
Julkaisukanavan avoimuus : Kokonaan avoin julkaisukanava
Verkko-osoite: https://doi.org/10.1016/j.isci.2025.113879
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/505587108
Morphogenesis of the cardiovascular system is responsive to hemodynamic cues sensed by endothelial cells. The organization of morphogenic signaling proteins is regulated by membrane presentation and internalization. Here, we aimed to characterize factors that regulate this flow-dependent protein localization by identifying differential interactors with the Notch ligand Jagged1 in response to shear stress. We cultured endothelial cells expressing Jagged1-APEX2 for proximity labeling on an orbital shaker shear stress platform. Myo1c was identified and confirmed through coimmunoprecipitation as a Jagged1-interacting factor under static conditions, with reduced interaction after exposure to shear. Jagged1 polarization downstream of shear followed by nucleograde transport was inhibited by Myo1c knockout. Further, Myo1c knockdown reduced membrane levels of Jagged1 under static but not shear conditions. Together, our data reveal a role for Myo1c in the hemodynamic control of Jagged1 localization in endothelial cells.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
Julkaisussa olevat rahoitustiedot:
This project has received funding from the European Research Council (ERC) under grant agreement number 771168 (ForceMorph) and the Academy of Finland under decision numbers 307133, 316882 (SPACE), 330411 (SignalSheets), and 336355 (strategic research profiling area Solutions for Health at Åbo Akademi University). The research has also been supported by the InFLAMES Flagship Programme of the Academy of Finland (decision numbers 337531, 357911, and 359346) and the Åbo Akademi University Foundation’s Center of Excellence in Cellular Mechanostasis (CellMech). K.L.L. was supported by the European Union’s Horizon 2020 research and innovation program under grant agreement 953234 (Tumor-LN-oC). F.S.R. was supported by The Swedish Cultural Foundation in Finland, Instrumentarium Science Foundation, and Magnus Ehrnrooth Foundation.
