磷酸化
IκB激酶
NF-κB
细胞生物学
αBκ
转录因子
炎症
激酶
信号转导
化学
肿瘤坏死因子α
NFKB1型
平衡
生物
免疫学
生物化学
基因
作者
Haifeng Wu,Hansen Liu,Xueying Zhao,Yi Zheng,Bingyu Liu,Lei Zhang,Chengjiang Gao
出处
期刊:Journal of Immunology
[American Association of Immunologists]
日期:2019-12-11
卷期号:204 (2): 418-427
被引量:29
标识
DOI:10.4049/jimmunol.1900626
摘要
Stringent regulation of the transcription factor NF-κB signaling is essential for the activation of host immune responses and maintaining homeostasis, yet the molecular mechanisms involved in its tight regulation are not completely understood. In this study, we report that IKK-interacting protein (IKIP) negatively regulates NF-κB activation. IKIP interacted with IKKα/β to block its association with NEMO, thereby inhibiting the phosphorylation of IKKα/β and the activation of NF-κB. Upon LPS, TNF-α, and IL-1β stimulation, IKIP-deficient macrophages exhibited more and prolonged IKKα/β phosphorylation, IκB, and p65 phosphorylation and production of NF-κB-responsive genes. Moreover, IKIP-deficient mice were more susceptible to LPS-induced septic shock and dextran sodium sulfate-induced colitis. Our study identifies a previously unrecognized role for IKIP in the negative regulation of NF-κB activation by inhibition of IKKα/β phosphorylation through the disruption of IKK complex formation.
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