KLF5相关文献与解析，生知库 | 链接生命科学的每一步

CRISPR screen of human pancreatic cancer xenografts identifies a KLF5 proliferation vulnerability through epigenetic modifiers NCAPD2 and MTHFD1.

通过 CRISPR 筛选人类胰腺癌异种移植瘤，发现 KLF5 增殖脆弱性与表观遗传修饰因子 NCAPD2 和 MTHFD1 有关。

Maeda Masahiro, Sherman Kenna, Zhou Weiqiang, Cheng Jiaqi, Nihongaki Yuta, Idrizi Adrian, Tryggvadottir Rakel, Camacho Oscar, Shang Xingbo, Min Jimin, Koldobskiy Michael A, Maitra Anirban, Levchenko Andre, Slusher Barbara S, Ji Hongkai, Feinberg Andrew P

胰腺癌

Ythdc1-p300-Klf5 Complex-Mediated Golgi Dysfunction Promotes Aortic Aneurysm.

Ythdc1-p300-Klf5复合物介导的高尔基体功能障碍促进主动脉瘤的发生。

期刊:Advanced Science

影响因子:14.1

doi:10.1002/advs.202512116

Wang Wen-Li, Song Zhi-Xue, Bu Si-Ming, Liu Yi-Mei, Li Qing, Zhang Wen-Xia, Sun Xu-Rong, Zhang Xin, Xiao Yu-Xuan, Bo Di, Miao Xu-Bin, Liu Chao, Zhang Xin-Hua, Zheng Lei, Zhao Hong-Ye, Zhang Bao-Lian, Jia Wen, Chi Kui, Liu Yu, Zhao Yong-Bo, Zheng Bin, Ma Dong, Wen Jin-Kun

KLF5 controls subtype-independent highly interactive enhancers in pancreatic cancer to regulate cell survival.

KLF5 控制胰腺癌中与亚型无关的高度相互作用的增强子，从而调节细胞存活。

期刊:Science Advances

影响因子:12.5

doi:10.1126/sciadv.aea2106

Tryptophan metabolic gatekeeping in epithelial repair: GPR35-KLF5 circuitry decodes mucosal damage signals for repair programming

色氨酸代谢调控在表皮修复中的作用：GPR35-KLF5 回路解码黏膜损伤信号以启动修复程序

期刊:Cell Death & Disease

影响因子:9.6

doi:10.1038/s41419-025-08237-0

Xie, Biao; Wang, Meimei; Xiao, Yaping; Zhang, Xin; Liu, Meng; Miao, Jie; Mo, Yunfei; Liu, Hongxin; Wang, Jihui; Xu, Fengguo; Wang, Di

Integrative multi-omics dissection identifies ACO2, KLF5, and IMP4 as central regulators of the mitochondrial-immune axis in ulcerative colitis

整合多组学分析鉴定出 ACO2、KLF5 和 IMP4 是溃疡性结肠炎中线粒体-免疫轴的核心调节因子

期刊:Frontiers in Immunology

影响因子:5.9

doi:10.3389/fimmu.2026.1746810

Tian, Yuanyuan; Qin, Xiaori; Li, Shibing; Wang, Jiao; Lan, Cheng

Multi-scale systems toxicology defines a KLF5-centered adverse outcome pathway linking DEHP exposure to pancreatic cancer progression and signaling programs relevant to therapy tolerance

多尺度系统毒理学定义了一条以 KLF5 为中心的毒性结局通路，该通路将 DEHP 暴露与胰腺癌进展以及与治疗耐受性相关的信号通路联系起来。

期刊:Frontiers in Cell and Developmental Biology

影响因子:4.3

doi:10.3389/fcell.2026.1769023

Chen, Jihao; Pang, Huaxin; Wang, Jundan; Guo, Junhua; Huang, Ting; Zhou, Heran

Targeting the undruggable transcription factor, KLF5, with a peptidomimetic small molecule, NC114, attenuates pressure overload-induced cardiac remodeling and fibrosis.

利用肽模拟小分子 NC114 靶向不可成药的转录因子 KLF5，可减轻压力超负荷引起的心脏重塑和纤维化。

期刊:Scientific Reports

影响因子:3.9

doi:10.1038/s41598-025-32155-y

Methatham Thanachai, Kimura Natsuka, Tomida Shota, Ishima Tamaki, Taguchi Yuki, Uosaki Hideki, Sakashita Eiji, Endo Hitoshi, Nagai Ryozo, Aizawa Kenichi

AGEs promote the metastasis of colorectal cancer cells via centrosome amplification by KLF5-CEP57L1 axis.

AGEs通过KLF5-CEP57L1轴介导的中心体扩增促进结直肠癌细胞的转移。

期刊:Journal of Biological Chemistry

影响因子:3.9

doi:10.1016/j.jbc.2025.111098

G-CSF promotes H3K27ac-modified KLF5 to activate CXCR4 expression and drive colon cancer growth and metastasis.

G-CSF 促进 H3K27ac 修饰的 KLF5 激活 CXCR4 表达，从而驱动结肠癌的生长和转移。

期刊:European Journal of Medical Research

影响因子:3.4

doi:10.1186/s40001-025-03613-0

Ma Guoqing, Jiang Jing, He Tingting, Jin Canhui, Wu Wenhao, Fan Wufeng, Wang Tianbao, Zhou Ping

A KLF5's domino effect drives metastatic pancreatic cancer

KLF5的多米诺效应驱动转移性胰腺癌

CRISPR screen of human pancreatic cancer xenografts identifies a KLF5 proliferation vulnerability through epigenetic modifiers NCAPD2 and MTHFD1.

通过 CRISPR 筛选人类胰腺癌异种移植瘤，发现 KLF5 增殖脆弱性与表观遗传修饰因子 NCAPD2 和 MTHFD1 有关。

Ythdc1-p300-Klf5 Complex-Mediated Golgi Dysfunction Promotes Aortic Aneurysm.

Ythdc1-p300-Klf5复合物介导的高尔基体功能障碍促进主动脉瘤的发生。

KLF5 controls subtype-independent highly interactive enhancers in pancreatic cancer to regulate cell survival.

KLF5 控制胰腺癌中与亚型无关的高度相互作用的增强子，从而调节细胞存活。

Tryptophan metabolic gatekeeping in epithelial repair: GPR35-KLF5 circuitry decodes mucosal damage signals for repair programming

色氨酸代谢调控在表皮修复中的作用：GPR35-KLF5 回路解码黏膜损伤信号以启动修复程序

Integrative multi-omics dissection identifies ACO2, KLF5, and IMP4 as central regulators of the mitochondrial-immune axis in ulcerative colitis

整合多组学分析鉴定出 ACO2、KLF5 和 IMP4 是溃疡性结肠炎中线粒体-免疫轴的核心调节因子

Multi-scale systems toxicology defines a KLF5-centered adverse outcome pathway linking DEHP exposure to pancreatic cancer progression and signaling programs relevant to therapy tolerance

多尺度系统毒理学定义了一条以 KLF5 为中心的毒性结局通路，该通路将 DEHP 暴露与胰腺癌进展以及与治疗耐受性相关的信号通路联系起来。

Targeting the undruggable transcription factor, KLF5, with a peptidomimetic small molecule, NC114, attenuates pressure overload-induced cardiac remodeling and fibrosis.

利用肽模拟小分子 NC114 靶向不可成药的转录因子 KLF5，可减轻压力超负荷引起的心脏重塑和纤维化。

AGEs promote the metastasis of colorectal cancer cells via centrosome amplification by KLF5-CEP57L1 axis.

AGEs通过KLF5-CEP57L1轴介导的中心体扩增促进结直肠癌细胞的转移。

G-CSF promotes H3K27ac-modified KLF5 to activate CXCR4 expression and drive colon cancer growth and metastasis.

G-CSF 促进 H3K27ac 修饰的 KLF5 激活 CXCR4 表达，从而驱动结肠癌的生长和转移。