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Loss of Histone Methyltransferase Ezh2 Exacerbates Polarization of Macrophages toward M2-Like Phenotypes by Hepatocellular Carcinoma

NIAID Data Ecosystem2026-05-10 收录

巨噬细胞M2极化

肝细胞癌免疫调控

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The raw, unadjusted, uncropped Western blot with size markers for the Western blot data

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创建时间：

2025-12-18

巨噬细胞M2极化

KLF4SUMO化调控

Macrophages, in response to different environmental cues, undergo the classical polarization (M1 macrophages) as well as the alternative polarization (M2 macrophages) that involve the functions of sti

NIAID Data Ecosystem40

MAPKAP kinase-2 Drives Expression of Angiogenic Factors by Tumor-Associated Macrophages in a Model of Inflammation-Induced Colon Cancer

巨噬细胞M2极化

结肠癌血管生成

MK2 is essential for optimal macrophage differentiation into a pro-tumorigenic M2-like state. Overall design: RNA-seq were performed on M0 and M2 polarized macrophages isolated from bone marrow of MK2

NIAID Data Ecosystem30

PERK is a critical metabolic hub for immunosuppressive function in macrophages

巨噬细胞M2极化

免疫代谢

Here we report that the Th2 cytokine IL-4 and the tumor microenvironment activated protein kinase RNA-like ER kinase (PERK) stress signaling cascade to promote immunosuppressive M2 activation and prol

NIAID Data Ecosystem10

Emodin inhibits macrophage alernative activation [Control-IL4-Emodin]

巨噬细胞M2极化

Emodin免疫调节

In order to fully characterize emodin's effects on macrophage alternative activation, peritoneal macrophages were stimulated with IL4 with or without emodin and gene expression was analyzed using a wh

NIAID Data Ecosystem40

IL-6 produced by prostate epithelial cells stimulated with Trichomonas vaginalis promotes proliferation of prostate cancer cells by inducing M2 polarization of THP-1-derived macrophages

肿瘤微环境

巨噬细胞M2极化

Trichomonas vaginalis (Tv), a protozoan parasite causing sexually-transmitted disease, has been detected in tissue of prostatitis, benign prostatic hyperplasia (BPH) and prostate cancer (PCa). IL-6, a

NIAID Data Ecosystem30

Loss of Histone Methyltransferase Ezh2 Exacerbates Polarization of Macrophages toward M2-Like Phenotypes by Hepatocellular Carcinoma

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