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

Employing epigenetic protein degradation techniques to block CCL5-mediated photodynamic therapy via a programmed delivery platform.

利用表观遗传蛋白降解技术,通过程序化递送平台阻断 CCL5 介导的光动力疗法。

Yang Tingting, Hu Yuzhu, Guo Anjie, Zhang Xifeng, Wang Wanyu, Yi Linbin, Zhang Rui, Gou Xinyu, Qian Zhiyong, Wang Bilan, Cheng Yongzhong, Gao Xiang

CCR1(hi)/CCL5(hi) macrophage-mediated CCL5(hi) T cell chemotaxis in salivary gland aggravates Sjögren's syndrome

唾液腺中CCR1(hi)/CCL5(hi)巨噬细胞介导的CCL5(hi)T细胞趋化作用会加重干燥综合征。

Zhou, Jiannan; Huang, Yingyi; Xiao, Di; Liu, Danyang; Chen, Xiaoying; Pan, Zehao; Wang, Lijing; Watanabe, Nobumoto; Pathak, Janak L; Li, Jiang

CCL5 promotes angiotensin II-induced cardiac remodeling through regulation of platelet-driven M2 macrophage polarization

CCL5通过调节血小板驱动的M2巨噬细胞极化促进血管紧张素II诱导的心脏重塑

Silin Lv ,Mingxuan Zhou ,Tiegang Li ,Zifan Zeng ,Zheng Yan ,Yufang Hou ,Liu Yang ,Fang Zhang ,Wenyi Zhao ,Yixin Zhou ,Min Yang

CCL5/RANTES signaling in inflammation dysregulation after mild traumatic brain injury.

轻度创伤性脑损伤后炎症失调中的 CCL5/RANTES 信号传导。

Ho Man-Hau, Tsai Yih-Jeng, Lee Yu-Hsuan, Hsieh Yi-Chen, Yen Chia-Hung, Wang Jia-Yi, Burnouf Thierry, Chen Chia-Yen, Lin Wen-Cheng, Wang Yun, Chiang Yung-Hsiao, Hoffer Barry J, Chou Szu-Yi

PP4 modulates macrophage-neutrophil crosstalk to restrict CCL5 -driven NETosis in sepsis.

PP4 调节巨噬细胞-中性粒细胞相互作用,从而限制脓毒症中 CCL5 驱动的 NETosis。

Yang Feng-Ming, Hsu Shih-Chang, Wu Yu-Chih, Chen Ching-Lu, Tan Tse-Hua, Chou Szu-Yi, Chang Hui-Ming, Yeh Edward T H

Astrocytic CCL5 orchestrates CCR5-positive neuronal necroptosis in subarachnoid hemorrhage.

星形胶质细胞 CCL5 调控蛛网膜下腔出血中 CCR5 阳性神经元的坏死性凋亡。

High-dose irradiation promotes macrophage-mediated engulfment of triple-negative breast cancer through M1 polarization via the IKZF1-CCL5 axis.

高剂量辐射通过 IKZF1-CCL5 轴促进巨噬细胞介导的 M1 极化,从而吞噬三阴性乳腺癌。

Kuo Han-Hsi, Chan Hui-Wen, Liu Chun-Yu, Chen Ming-Huang, Lee Yi-Jang, Chuang Hui-Yen, Chang Yu-Chan

CCL5 deficiency aggravates acute DSS-induced colitis by restricting IL-33-induced formation of Tregs in intestinal tract.

CCL5 缺乏会通过限制肠道中 IL-33 诱导的 Treg 形成来加重急性 DSS 诱导的结肠炎。

Luo Yang, Gong Ting-Yue, Zhao Yong-Heng, Li Hao, Ye Guang-Yao, Zhang Zi-Zhen, Yu Min-Hao, Zhang Yan, Zhong Ming

Folate promotes colorectal cancer progression by impairing CD8(+) T cell function and recruitment via SLC19A1/p-AKT/NOTCH1 axis and CCL5 downregulation

叶酸通过SLC19A1/p-AKT/NOTCH1轴和CCL5下调抑制CD8(+) T细胞的功能和募集,从而促进结直肠癌的进展。

Qing, Shunjie; Ling, Yunyan; Lai, Yingjie; Hu, Yating; Zhong, Yi; Liu, Yuechen; Liu, Xiang; Fang, Yuan; Qian, Junying; Deng, Haijun; Peng, Yifeng; Wu, Dehua; Shen, Zhiyong

ANGPTL8 links refeeding to monocyte dynamics and metabolic inflammation via the CCL5-CCR5 axis.

ANGPTL8 通过 CCL5-CCR5 轴将再喂养与单核细胞动力学和代谢炎症联系起来。