5UKE

NMR structure of monomeric human IRAK-M Death Domain R56D, Y61E mutant

5UKE の概要

• エントリーDOI: 10.2210/pdb5uke/pdb
• NMR情報: BMRB: 30237
• 分子名称: Interleukin-1 receptor-associated kinase 3 (1 entity in total)
• 機能のキーワード: irak-m, death domain, innate immunity, asthma, transferase
• 由来する生物種: Homo sapiens (Human)
• タンパク質・核酸の鎖数: 1
• 化学式量合計: 13467.16

構造登録者

Kwon, J.,Nicholson, L.K. (登録日: 2017-01-20, 公開日: 2018-01-24, 最終更新日: 2024-05-01)

主引用文献

Nechama, M.,Kwon, J.,Wei, S.,Kyi, A.T.,Welner, R.S.,Ben-Dov, I.Z.,Arredouani, M.S.,Asara, J.M.,Chen, C.H.,Tsai, C.Y.,Nelson, K.F.,Kobayashi, K.S.,Israel, E.,Zhou, X.Z.,Nicholson, L.K.,Lu, K.P.
The IL-33-PIN1-IRAK-M axis is critical for type 2 immunity in IL-33-induced allergic airway inflammation.
Nat Commun, 9:1603-1603, 2018

PubMed Abstract: Interleukin 33 (IL-33) is among the earliest-released cytokines in response to allergens that orchestrate type 2 immunity. The prolyl cis-trans isomerase PIN1 is known to induce cytokines for eosinophil survival and activation by stabilizing cytokines mRNAs, but the function of PIN1 in upstream signaling pathways in asthma is unknown. Here we show that interleukin receptor associated kinase M (IRAK-M) is a PIN1 target critical for IL-33 signaling in allergic asthma. NMR analysis and docking simulations suggest that PIN1 might regulate IRAK-M conformation and function in IL-33 signaling. Upon IL-33-induced airway inflammation, PIN1 is activated for binding with and isomerization of IRAK-M, resulting in IRAK-M nuclear translocation and induction of selected proinflammatory genes in dendritic cells. Thus, the IL-33-PIN1-IRAK-M is an axis critical for dendritic cell activation, type 2 immunity and IL-33 induced airway inflammation.

PubMed: 29686383
DOI: 10.1038/s41467-018-03886-6

実験手法

SOLUTION NMR