日期:
2020 年 — 2026 年
2020
2021
2022
2023
2024
2025
2026
影响因子:

Tgm2-Catalyzed Covalent Cross-Linking of IκBα Drives NF-κB Nuclear Translocation to Promote SASP in Senescent Microglia

Tgm2催化的IκBα共价交联驱动NF-κB核转位,从而促进衰老小胶质细胞中的SASP

Zhiqiang Li ,Tianxiang Wang ,Sijing Du ,Zelong Miao ,Yujiao Zhao ,Yuxiang Tang ,Xianbin Meng ,Shangcheng Yu ,Dongyuan Zhang ,Hao Jiang ,Kunlin Du ,Wei Wei ,Haiteng Deng

Dual-specific autophosphorylation of kinase IKK2 enables phosphorylation of substrate IκBα through a phosphoenzyme intermediate

激酶 IKK2 的双特异性自磷酸化可通过磷酸酶中间体实现底物 IκBα 的磷酸化。

Prateeka Borar ,Tapan Biswas # ,Ankur Chaudhuri # ,Pallavi T Rao ,Swasti Raychaudhuri ,Tom Huxford ,Saikat Chakrabarti ,Gourisankar Ghosh ,Smarajit Polley

Spatiotemporal dynamics of NF-κB/Dorsal inhibitor IκBα/Cactus in Drosophila blastoderm embryos

果蝇胚盘胚胎中NF-κB/Dorsal抑制因子IκBα/Cactus的时空动态

Allison E Schloop ,Sharva Vijayakumar Hiremath ,Razeen Shaikh ,Sadia Siddika Dima ,Leslie Lizardo ,Amrit Bhakta ,Cranos M Williams ,Gregory T Reeves

Overexpression of Foxc1 ameliorates sepsis‑associated encephalopathy by inhibiting microglial migration and neuroinflammation through the IκBα/NF‑κB pathway

Foxc1 过表达可通过 IκBα/NF-κB 通路抑制小胶质细胞迁移和神经炎症,从而改善脓毒症相关性脑病。

Hongyu Wang ,Hongwei Wang ,Yinsen Song ,Congyan Liu ,Xinling Qian ,Dalong Zhang ,Xin Jiang ,Sisen Zhang

Evaluation of the osteogenic effect of apigenin on human mesenchymal stem cells by inhibiting inflammation through modulation of NF-κB/IκBα

通过调节 NF-κB/IκBα 抑制炎症,评价芹菜素对人骨髓间充质干细胞的成骨作用

Azita Asadi ,Farjam Goudarzi ,Mustafa Ghanadian ,Adel Mohammadalipour

Low-Dose Decitabine Augments the Activation and Anti-Tumor Immune Response of IFN-γ+ CD4+ T Cells Through Enhancing IκBα Degradation and NF-κB Activation

低剂量地西他滨通过增强IκBα降解和NF-κB活化来增强IFN-γ+CD4+T细胞的活化和抗肿瘤免疫反应

Xiang Li,Liang Dong,Jiejie Liu,Chunmeng Wang,Yan Zhang,Qian Mei,Weidong Han,Ping Xie,Jing Nie

Synergistic activation of NF-kappaB by tumor necrosis factor alpha and gamma interferon via enhanced I kappaB alpha degradation and de novo I kappaBbeta degradation

肿瘤坏死因子α和γ干扰素通过增强IκBα降解和从头合成IκBβ降解,协同激活NF-κB。

J L Cheshire ,A S Baldwin Jr