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

EGFR inhibitor-resistant lung cancers exhibit collateral sensitivity to a covalent, cysteine-independent KEAP1 oligomerizing molecular bridge.

对 EGFR 抑制剂耐药的肺癌表现出对共价、不依赖半胱氨酸的 KEAP1 寡聚化分子桥的协同敏感性。

Bassil Christopher F, Dillon Kerry, Anderson Gray R, Mayro Benjamin, Askin Kayleigh N, Winter Peter S, Harry Stefan, Gruber Samuel, Hall Tierney M, Hoj Jacob P, Cerda-Smith Christian, Hutchinson Haley M, Killarney Shane T, Heffernan Ava, Teddy Caroline, Singleton Katherine R, Qin Li, Jubien-Girard Kévin, Favreau Cécile, Robert Guillaume, Tivon Barr, Livnah Ella, London Nir, Benhida Rachid, Auberger Patrick, Pendergast Ann Marie, Bar-Peled Liron, Lonard David M, Martin Anthony R, Puissant Alexandre, Wood Kris C

Differential KEAP1/NRF2 mediated signaling widens the therapeutic window of redox-targeting drugs in SCLC therapy.

KEAP1/NRF2 介导的差异性信号传导拓宽了小细胞肺癌治疗中氧化还原靶向药物的治疗窗口。

Samarin Jana, Nůsková Hana, Fabrowski Piotr, Malz Mona, Amtmann Eberhard, Taeubert Minerva J, Pastor-Flores Daniel, Kazdal Daniel, Kurilov Roman, de Vries Nicole, Pink Hannelore, Deis Franziska, Hummel-Eisenbeiss Johanna, Renz Lisa, Kaushal Kamini, Morgen Michael, Dick Tobias P, Hamilton Gerhard, Muckenthaler Martina, Mall Moritz, Lim Bryce, Kanamaru Taishi, Klinke Glynis, Sos Martin L, Frede Julia, Miller Aubry K, Alborzinia Hamed, Gunkel Nikolas

Tussilagone attenuated cigarette smoke-induced chronic obstructive pulmonary disease through regulating Nrf2 and NF-κB/NLRP3 inflammasome via directly targeting cysteine 434 of KEAP1.

Tussilagone 通过直接靶向 KEAP1 的半胱氨酸 434 来调节 Nrf2 和 NF-κB/NLRP3 炎症小体,从而减轻香烟烟雾引起的慢性阻塞性肺病。

Corrigendum to "KEAP1 C151 active site catalysis drives electrophilic signaling to upregulate cytoprotective enzyme expression" [Redox Biology 88 (2025) 103906]

对“KEAP1 C151 活性位点催化驱动亲电信号上调细胞保护酶表达”的更正 [Redox Biology 88 (2025) 103906]

Schnell, Matthew R; Zhai, Tianhua; Ragwan, Edwin R; Jung, Hannah; Zhang, Jiayu; Lagalante, Anthony F; Kung, Yan; Kraut, Daniel A; Huang, Zuyi; Eggler, Aimee L

UFMylation deficiency in hepatocytes activates the KEAP1-NRF2 pathway and contributes to hepatocarcinogenesis.

肝细胞中UFMylation缺乏会激活KEAP1-NRF2通路,并促进肝癌的发生。

Liang Qian, Xu Shiwen, Fang Yaoyao, Wang Xue, Xiao Yang, Wang Yiwen, Li Shujuan, Guo Qifan, Cao Yu, Cao Ying, Liu Chao, Zhao Yuqin, Luo Yan, Wu Anqi, Wang Miao, Shi Junping, Li Guoqing, Cong Yu-Sheng

A novel biomimetic nanozyme orchestrates ulcerative colitis resolution by targeting KEAP1-NRF2-ARE pathway: Redox balance restoration, colonic barrier repair, immune homeostasis regulation.

一种新型仿生纳米酶通过靶向 KEAP1-NRF2-ARE 通路来协调溃疡性结肠炎的消退:恢复氧化还原平衡、修复结肠屏障、调节免疫稳态。

Gong Ping, Wang Yuqi, Qiu Jia-He, Li Guanghui, Chen Ke-Wei, Li Zhuoya, Wang Xi, Wang Liping

TM4SF5-mediated KEAP1 Regulation in Hepatocytes Irrelevant to NRF2 Expression and Activity Promotes Oxidative Stress and Inflammation to Develop Metabolic Dysfunction-Associated Steatotic Liver Disease.

TM4SF5介导的肝细胞KEAP1调控与NRF2表达和活性无关,促进氧化应激和炎症,从而发展为代谢功能障碍相关的脂肪肝疾病。

Shin Eun-Ae, Lee Haesong, Pyo Kyung-Hee, Kim Wonsik, Kim Soyeon, Lee Jae-Ho, Jin Seo Hee, Kim Eunmi, Byeon Soo-Min, Kim Dong Joo, Cho Young Jun, Kim Tae Won, Ohn Minjae, Lee Hyojung, Lee Jeongwon, Jeong Jinwook, Kim Doojin, Zheng Jie, Lee Han Ah, Kim Hwi Young, Surh Young-Joon, Lee Jung Weon

Combinatorial use of VHL and KEAP1 PROTACs reveals unexpected synergy and hook effect relief.

VHL 和 KEAP1 PROTAC 的组合使用揭示了意想不到的协同作用和钩状效应缓解。

CILP Inhibits hyaline cartilage fibrosis and chondrocyte ferroptosis via keap1-Nrf2 axis in early osteoarthritis exercise therapy.

CILP 通过 keap1-Nrf2 轴抑制早期骨关节炎运动疗法中的透明软骨纤维化和软骨细胞铁死亡。

Jia Shuangshuo, Hu Zhehan, Li Zihan, Zhang Weiming, Chen Liang, Niu Changping, Zhao Ziqi, Sun Yuhan, Yao Gang, Wang Yang, Yang Yue

Methotrexate-triggered ferroptosis suppresses oral cancer progression by phosphorylated KEAP1-mediated NRF2 degradation to inhibit SLC7A11/GPX4 signaling pathway.

甲氨蝶呤触发的铁死亡通过磷酸化 KEAP1 介导的 NRF2 降解来抑制 SLC7A11/GPX4 信号通路,从而抑制口腔癌的进展。

Yu Chenchen, Zhang Tingting, Yuan Jialu, Su Yijing, Zhang Hongli, Xu Liqin, Li Xiaomin, Cui Jianan, Xu Rui, Zhou Yan, Huang Hongming, Zhou Xiaorong, Zhou Yongqiang, Zhang Erhao