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Transcription profiling of mouse lipopolysaccharide-induced inflammation in HFE-deficient and wild types

ChEBI2004-03-15 更新2026-07-21 收录

炎症分子机制

遗传性血色素沉着病模型

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-MEXP-95 数据链接链接失效反馈

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资源简介：

Transcription profiling of mouse lipopolysaccharide-induced inflammation in HFE-deficient and wild types

应用场景：

创建时间：

2004-03-15

炎症分子机制

TLR4/MD-2信号通路

The cytosolic Ca2+-binding S100A9 and S100A8 proteins form heterodimers that are primarily expressed in human neutrophils and monocytes. We have recently shown that S100A9 binds to TLR4 in vitro and i

NIAID Data Ecosystem90

ORP8 KO BMDMs have reduced excretion of pro-inflammatory cytokines and reduced expression of co-stimulatory factors.

免疫调节

炎症分子机制

Bone Marrow-Derived Macrophages (BMDMs) were generated from bone marrow of ORP8 KO mice or WT controls and stimulated with LPS (100 ng/mL). A) A decrease in secretion of IL-6 by LPS stimulated ORP8 KO

NIAID Data Ecosystem80

Epigenomic and transcriptomic differences between low-grade and acute inflammation in LPS-induced murine immune cells

炎症分子机制

TLR4信号通路

Chronic, low-grade inflammation has a widespread and significant impact on health, especially in Western-society. While inflammation is beneficial for the removal of microbes, low-grade inflammation n

NIAID Data Ecosystem50

Effect of lipopolysachharide (LPS) on the expression of microRNAs (miRNAs) in the mouse oviduct. Mus musculus

生殖系统miRNA表达

炎症分子机制

Our objective was to determine the effect of intraperitoneal (IP) administration of E. Coli-derived lipopolysaccharide (LPS) on the acute expression of miRNAs in the mouse oviduct Overall design: On t

NIAID Data Ecosystem80

miRNA array for LPS-activated tnc+/+ and tnc-/- macrophages

巨噬细胞免疫调节

炎症分子机制

Endogenous molecules generated upon pathogen invasion or tissue damage serve as danger signals that activate host defence, however their precise immunological role remains unclear. Tenascin-C is an ex

NIAID Data Ecosystem50

Transcription profiling of mouse lipopolysaccharide-induced inflammation in HFE-deficient and wild types

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