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Publication : YTHDF1-CLOCK axis contributes to pathogenesis of allergic airway inflammation through LLPS.

First Author  Wang J Year  2024
Journal  Cell Rep Volume  43
Issue  3 Pages  113947
PubMed ID  38492220 Mgi Jnum  J:352908
Mgi Id  MGI:7616021 Doi  10.1016/j.celrep.2024.113947
Citation  Wang J, et al. (2024) YTHDF1-CLOCK axis contributes to pathogenesis of allergic airway inflammation through LLPS. Cell Rep 43(3):113947
abstractText  N6-methyladenosine (m6A) modification has been implicated in many cell processes and diseases. YTHDF1, a translation-facilitating m6A reader, has not been previously shown to be related to allergic airway inflammation. Here, we report that YTHDF1 is highly expressed in allergic airway epithelial cells and asthmatic patients and that it influences proinflammatory responses. CLOCK, a subunit of the circadian clock pathway, is the direct target of YTHDF1. YTHDF1 augments CLOCK translation in an m6A-dependent manner. Allergens enhance the liquid-liquid phase separation (LLPS) of YTHDF1 and drive the formation of a complex comprising dimeric YTHDF1 and CLOCK mRNA, which is distributed to stress granules. Moreover, YTHDF1 strongly activates NLRP3 inflammasome production and interleukin-1beta secretion leading to airway inflammatory responses, but these phenotypes are abolished by deleting CLOCK. These findings demonstrate that YTHDF1 is an important regulator of asthmatic airway inflammation, suggesting a potential therapeutic target for allergic airway inflammation.
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